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April 30, 2006
Socially Active Elderly Suffered Less Neurological Damage, Study Found
FRIDAY, April 28 (HealthDay News) -- Social networks -- such as having close friends and staying in contact with family members -- help protect against the damaging effects of Alzheimer's disease, a new U.S. study finds.
"Many elderly people who have the tangles and plaques associated with Alzheimer's disease don't clinically experience cognitive impairment or dementia," Dr. David A. Bennett of the Rush University Medical Center's Alzheimer's Disease Center, Chicago, said in a prepared statement. "Our findings suggest that social networks are related to something that offers a 'protective reserve' capacity that spares them the clinical manifestations of Alzheimer's disease," he said.
The study included 89 elderly people without known dementia taking part in the Rush Memory and Aging Project. While they were alive, each provided information about their social networks and underwent 21 cognitive performance tests each year. After they died, their brains were analyzed.
The larger a person's social network, the less effect the tangles and plaques had on their cognitive test scores. This protective effect was noted across different kinds of cognitive abilities but was most evident for semantic memory, which contains knowledge about the world and is involved in language and other uniquely human cognitive processes.
The study currently appears online in The Lancet Neurology and is expected to be published in the May print issue of the journal.
"Identifying factors associated with the ability to tolerate the pathology of Alzheimer's has important implications for disease prevention," Bennett said. "Previous studies suggest one factor is education. Now we know that healthy and frequent interactions with friends and family have a positive impact as well," he added.
Source: Robert Preidt. Full Social Lives May Protect Against Alzheimer's. Foodconsumer.org (29 April 2006) [FullText]
"Many elderly people who have the tangles and plaques associated with Alzheimer's disease don't clinically experience cognitive impairment or dementia," Dr. David A. Bennett of the Rush University Medical Center's Alzheimer's Disease Center, Chicago, said in a prepared statement. "Our findings suggest that social networks are related to something that offers a 'protective reserve' capacity that spares them the clinical manifestations of Alzheimer's disease," he said.
The study included 89 elderly people without known dementia taking part in the Rush Memory and Aging Project. While they were alive, each provided information about their social networks and underwent 21 cognitive performance tests each year. After they died, their brains were analyzed.
The larger a person's social network, the less effect the tangles and plaques had on their cognitive test scores. This protective effect was noted across different kinds of cognitive abilities but was most evident for semantic memory, which contains knowledge about the world and is involved in language and other uniquely human cognitive processes.
The study currently appears online in The Lancet Neurology and is expected to be published in the May print issue of the journal.
"Identifying factors associated with the ability to tolerate the pathology of Alzheimer's has important implications for disease prevention," Bennett said. "Previous studies suggest one factor is education. Now we know that healthy and frequent interactions with friends and family have a positive impact as well," he added.
Source: Robert Preidt. Full Social Lives May Protect Against Alzheimer's. Foodconsumer.org (29 April 2006) [FullText]
posted by Dr. Koudinov @ 30.4.06
0 comments
April 25, 2006
Apathy and Its Treatment in Alzheimer's Disease
"Although memory and other cognitive impairments are considered the hallmark features of most dementias, neuropsychiatric abnormalities occur in the majority of such patients (Cohen et al., 1993). Neuropsychiatric symptoms are associated with a rapid course of decline, elevated caregiver distress and overutilization of health care services (Chung and Cummings, 2000; Teri, 1997). Apathy is the most common neuropsychiatric symptom reported among individuals with Alzheimer's disease (AD), affecting approximately 70% of patients in the mild-to-moderate stages (Landes et al., 2001) and increasing in severity as the illness progresses (Mega et al., 1996). Apathy is common in other dementing illnesses as well (e.g., Parkinson's disease [PD], vascular dementia) and may even occur in substantial numbers of patients with mild cognitive impairment (Ready et al., 2003). Apathy is associated with functional impairment and caregiver distress at all levels of disease severity (Boyle et al., 2003; Norton et al., 2001; Rymer et al., 2002).
Apathy is characterized by the loss of initiation and motivation to participate in activities, social withdrawal, and emotional indifference (Marin, 1991). Depression shares some overlapping features (e.g., decreased initiation, social withdrawal), but can be distinguished from apathy primarily on the basis of dysphoria (Marin et al., 1994). Symptoms of dysphoria typically are absent in the apathetic patient, who displays a lack of interest and motivation in the context of emotional indifference. Apathy therefore reflects a syndrome of primary motivational loss, whereas depression reflects a primary mood disturbance.
The Neurobiological Basis
Although the neurobiological basis of apathy remains to be fully elucidated, dysfunction in frontal systems is thought to be important. Three subsystems of the frontal lobes are thought to underlie three distinct neuropsychiatric syndromes: 1) The dorsolateral prefrontal circuit is associated with executive cognitive dysfunction; 2) The lateral orbital prefrontal circuit is associated with disinhibition; and 3) The medial (anterior cingulate) circuit is associated with disorders of motivation, including apathy (Cummings, 1993). In the extreme, large bilateral lesions in the anterior cingulate cortex produce akinetic mutism, a state of profound apathy and amotivational immobility. Neuropathological changes in dementia may result in apathy by affecting this medial frontal circuit, as well as parietotemporal brain regions that subserve motivation and emotion. Cummings and Back (1998) have also proposed that medial frontal and limbic cholinergic deficits may underlie apathy. Dopaminergic pathways that influence frontal-subcortical activation may also play a role in apathy.
Apathy Assessment
A number of instruments have been developed for assessing neuropsychiatric symptoms in individuals with dementia (Table).
The Neuropsychiatric Inventory (NPI) is the most widely used instrument for assessing neuropsychiatric functioning in patients with dementia (Cummings et al., 1994). It is a valid and reliable instrument involving a caregiver interview designed to assess the presence and severity of 10 symptoms: apathy, irritability/lability, dysphoria, delusions, hallucinations, anxiety, agitation/aggression, euphoria, disinhibition and aberrant motor activity. Tekin et al. (2001) reported significant correlations between NPI apathy subscale scores and frontal pathology at autopsy in patients with AD, suggesting that the NPI is useful for this purpose. Moreover, the NPI includes apathy and depression items, which can help clinicians distinguish apathy from depression.
The Frontal Systems Behavior Scale (FrSBe) is a newer instrument that was specifically designed to measure behavioral changes related to frontal system dysfunction (Grace and Malloy, 2001). It is a valid, reliable, 46-item questionnaire that assesses the three frontal behavioral syndromes linked to the frontal circuits described earlier: apathy, disinhibition and executive dysfunction. The FrSBe measure of apathy correlates moderately with the NPI apathy rating (Norton et al., 2001) and other ratings of decreased initiation (Ready et al., 2003), but not with the Geriatric Depression Scale (GDS) (Cahn-Weiner et al., 2002). The FrSBe correlates more highly with activities of daily living impairment than the NPI (Boyle et al., 2003; Norton et al., 2001).
The Apathy Evaluation Scale (AES)-Informant version is an 18-item, informant-rated scale that utilizes a four-point Likert-type scale to assess symptoms of apathy (Marin et al., 1991). Although it is widely used, there are very limited guidelines for interpreting AES scores, and Glenn et al. (2002) reported that the AES had poor sensitivity and specificity with respect to the ability to predict the clinician's designation of a patient as apathetic. The Apathy Inventory (IA) is a new instrument that generates scores for emotional blunting, lack of initiation and lack of interest, in addition to a global apathy score (Robert et al., 2002). Preliminary evidence suggests that the caregiver-rated version of the IA is valid and reliable, and total scores on the IA correlate well with the NPI apathy subscale, suggesting high concurrent validity (Robert et al., 2002). A recent review by Malloy and Grace (2005) provides further information on these and related scales.
Treating Apathy
Cholinesterase inhibitors have some efficacy for reducing the neuropsychiatric symptoms associated with dementia, and apathy is the neuropsychiatric symptom most consistently responsive to treatment (Cummings, 2003; Wynn and Cummings, 2004). Large-scale clinical trials have generally indicated that donepezil (Aricept) improves neuropsychiatric functioning, particularly the symptom of apathy (Birks and Harvey, 2003; Feldman et al., 2001; Gauthier et al., 2002; Trinh et al., 2003). A few studies also indicate that galantamine (Razadyne) and rivastigmine (Exelon) may also have beneficial neuropsychiatric effects (Birks et al., 2000). A placebo-controlled, double-blind study evaluated the effects of galantamine in AD patients with cerebrovascular disease and probable vascular dementia (Erkinjuntti, 2002). Researchers found that galantamine was associated with a significant reduction in apathy and anxiety over six-month follow-up. Dartigues et al. (2002) found that rivastigmine resulted in improvement in apathy, irritability, delusions and anxiety in patients with mild-to-moderate AD over a six-month follow-up.
Preliminary evidence also supports the use of activating pharmacologic agents for treating apathy in patients with dementia (Marin et al., 1995). Psychostimulants such as methylphenidate and dextroamphetamine (Dexedrine, DextroStat) have been shown to reduce symptoms of apathy in case series of patients with AD, PD or cerebrovascular disease (Chatterjee and Fahn, 2002; Galynker et al., 1997; Jansen et al., 2001). Given the phenomenological overlap between apathy and depression, nondepressed dementia patients with apathy may also benefit from the use of antidepressants with stimulant properties. Some evidence suggests that dopaminergic agents may also be useful for reducing apathy, perhaps through enhancement of the functioning of frontostriatal circuits (Corcoran et al., 2004; Muller and von Cramon, 1994; Newburn and Newburn, 2005). Controlled clinical trials are needed to demonstrate convincingly the effectiveness of stimulants, antidepressants and dopaminergic agents in treating apathy in dementia. Additional research is needed to determine the magnitude and duration of positive effect and ensure that reductions in apathy are not accompanied by increases in agitation, psychosis or other side effects. Our research group is currently conducting a double-blind, National Institute on Aging-sponsored study comparing cholinesterase inhibitors alone to cholinesterase inhibitors plus modafinil (Provigil) in the treatment of apathy.
Behavioral Interventions
Combined pharmacological-behavioral approaches have consistently been shown to be more effective than pharmacologic treatments alone in a wide variety of disorders, including depression. In dementia populations, behavior therapy and applied behavioral analysis techniques have been used successfully to improve such diverse problems as incontinence, agitation and aggression (Teri and Gallagher-Thompson, 1991). Although apathy has not been specifically addressed using behavioral interventions to date, evidence suggests that behavioral interventions are effective for treating depression in patients with AD and their caregivers (Teri et al., 1997). Behavioral interventions in dementia have also resulted in improved patient health and lower caregiver burden (Teri et al., 2003). We recently completed a controlled trial of the effectiveness of a novel caregiver-based behavioral training program for reducing apathy in patients with AD and reducing stress among their caregivers. Preliminary findings suggest that behavioral intervention benefited patients with AD and their caregivers (Boyle et al., 2004). Further research examining the benefits of combined, pharmacological-behavioral interventions is needed.
Summary and Conclusions
Apathy is a debilitating and underrecognized syndrome that affects the vast majority of individuals with dementia, results in functional impairment among patients and causes stress among their caregivers. Accurate discrimination of the symptoms of apathy from depression is necessary for optimal treatment. The careful comparison of the symptoms of dysphoria versus symptoms of amotivation is recommended, and a number of instruments have been developed to aid in the discrimination of apathy from depression.
Cholinesterase inhibitors have been shown to reduce the neuropsychiatric symptoms of AD and vascular dementia with apathy showing the most consistent gains. The magnitude and persistence of these changes remains a topic for future research. Traditional antidepressants, activating neurologic agents and combined pharmacological-behavioral treatments also hold promise for the treatment of apathy, but controlled large-scale clinical trials are lacking. For more detailed reviews, the reader is referred to Boyle and Malloy (2004) and Wynn and Cummings (2004).
Dr. Malloy is associate professor at Brown Medical School and co-director of the Butler Hospital Memory Disorders Program.
Dr. Boyle is a neuropsychologist with the Rush Alzheimer's Disease Center and assistant professor in the department of behavioral sciences at Rush University Medical Center.
Source: Paul F. Malloy, Ph.D., and Patricia A. Boyle, Ph.D. Apathy and Its Treatment in Alzheimer's Disease and Other Dementias. Psychiatric Times (2005) Vol. XXIII Issue 13 [FullText, References, and Images]
Apathy is characterized by the loss of initiation and motivation to participate in activities, social withdrawal, and emotional indifference (Marin, 1991). Depression shares some overlapping features (e.g., decreased initiation, social withdrawal), but can be distinguished from apathy primarily on the basis of dysphoria (Marin et al., 1994). Symptoms of dysphoria typically are absent in the apathetic patient, who displays a lack of interest and motivation in the context of emotional indifference. Apathy therefore reflects a syndrome of primary motivational loss, whereas depression reflects a primary mood disturbance.
The Neurobiological Basis
Although the neurobiological basis of apathy remains to be fully elucidated, dysfunction in frontal systems is thought to be important. Three subsystems of the frontal lobes are thought to underlie three distinct neuropsychiatric syndromes: 1) The dorsolateral prefrontal circuit is associated with executive cognitive dysfunction; 2) The lateral orbital prefrontal circuit is associated with disinhibition; and 3) The medial (anterior cingulate) circuit is associated with disorders of motivation, including apathy (Cummings, 1993). In the extreme, large bilateral lesions in the anterior cingulate cortex produce akinetic mutism, a state of profound apathy and amotivational immobility. Neuropathological changes in dementia may result in apathy by affecting this medial frontal circuit, as well as parietotemporal brain regions that subserve motivation and emotion. Cummings and Back (1998) have also proposed that medial frontal and limbic cholinergic deficits may underlie apathy. Dopaminergic pathways that influence frontal-subcortical activation may also play a role in apathy.
Apathy Assessment
A number of instruments have been developed for assessing neuropsychiatric symptoms in individuals with dementia (Table).
The Neuropsychiatric Inventory (NPI) is the most widely used instrument for assessing neuropsychiatric functioning in patients with dementia (Cummings et al., 1994). It is a valid and reliable instrument involving a caregiver interview designed to assess the presence and severity of 10 symptoms: apathy, irritability/lability, dysphoria, delusions, hallucinations, anxiety, agitation/aggression, euphoria, disinhibition and aberrant motor activity. Tekin et al. (2001) reported significant correlations between NPI apathy subscale scores and frontal pathology at autopsy in patients with AD, suggesting that the NPI is useful for this purpose. Moreover, the NPI includes apathy and depression items, which can help clinicians distinguish apathy from depression.
The Frontal Systems Behavior Scale (FrSBe) is a newer instrument that was specifically designed to measure behavioral changes related to frontal system dysfunction (Grace and Malloy, 2001). It is a valid, reliable, 46-item questionnaire that assesses the three frontal behavioral syndromes linked to the frontal circuits described earlier: apathy, disinhibition and executive dysfunction. The FrSBe measure of apathy correlates moderately with the NPI apathy rating (Norton et al., 2001) and other ratings of decreased initiation (Ready et al., 2003), but not with the Geriatric Depression Scale (GDS) (Cahn-Weiner et al., 2002). The FrSBe correlates more highly with activities of daily living impairment than the NPI (Boyle et al., 2003; Norton et al., 2001).
The Apathy Evaluation Scale (AES)-Informant version is an 18-item, informant-rated scale that utilizes a four-point Likert-type scale to assess symptoms of apathy (Marin et al., 1991). Although it is widely used, there are very limited guidelines for interpreting AES scores, and Glenn et al. (2002) reported that the AES had poor sensitivity and specificity with respect to the ability to predict the clinician's designation of a patient as apathetic. The Apathy Inventory (IA) is a new instrument that generates scores for emotional blunting, lack of initiation and lack of interest, in addition to a global apathy score (Robert et al., 2002). Preliminary evidence suggests that the caregiver-rated version of the IA is valid and reliable, and total scores on the IA correlate well with the NPI apathy subscale, suggesting high concurrent validity (Robert et al., 2002). A recent review by Malloy and Grace (2005) provides further information on these and related scales.
Treating Apathy
Cholinesterase inhibitors have some efficacy for reducing the neuropsychiatric symptoms associated with dementia, and apathy is the neuropsychiatric symptom most consistently responsive to treatment (Cummings, 2003; Wynn and Cummings, 2004). Large-scale clinical trials have generally indicated that donepezil (Aricept) improves neuropsychiatric functioning, particularly the symptom of apathy (Birks and Harvey, 2003; Feldman et al., 2001; Gauthier et al., 2002; Trinh et al., 2003). A few studies also indicate that galantamine (Razadyne) and rivastigmine (Exelon) may also have beneficial neuropsychiatric effects (Birks et al., 2000). A placebo-controlled, double-blind study evaluated the effects of galantamine in AD patients with cerebrovascular disease and probable vascular dementia (Erkinjuntti, 2002). Researchers found that galantamine was associated with a significant reduction in apathy and anxiety over six-month follow-up. Dartigues et al. (2002) found that rivastigmine resulted in improvement in apathy, irritability, delusions and anxiety in patients with mild-to-moderate AD over a six-month follow-up.
Preliminary evidence also supports the use of activating pharmacologic agents for treating apathy in patients with dementia (Marin et al., 1995). Psychostimulants such as methylphenidate and dextroamphetamine (Dexedrine, DextroStat) have been shown to reduce symptoms of apathy in case series of patients with AD, PD or cerebrovascular disease (Chatterjee and Fahn, 2002; Galynker et al., 1997; Jansen et al., 2001). Given the phenomenological overlap between apathy and depression, nondepressed dementia patients with apathy may also benefit from the use of antidepressants with stimulant properties. Some evidence suggests that dopaminergic agents may also be useful for reducing apathy, perhaps through enhancement of the functioning of frontostriatal circuits (Corcoran et al., 2004; Muller and von Cramon, 1994; Newburn and Newburn, 2005). Controlled clinical trials are needed to demonstrate convincingly the effectiveness of stimulants, antidepressants and dopaminergic agents in treating apathy in dementia. Additional research is needed to determine the magnitude and duration of positive effect and ensure that reductions in apathy are not accompanied by increases in agitation, psychosis or other side effects. Our research group is currently conducting a double-blind, National Institute on Aging-sponsored study comparing cholinesterase inhibitors alone to cholinesterase inhibitors plus modafinil (Provigil) in the treatment of apathy.
Behavioral Interventions
Combined pharmacological-behavioral approaches have consistently been shown to be more effective than pharmacologic treatments alone in a wide variety of disorders, including depression. In dementia populations, behavior therapy and applied behavioral analysis techniques have been used successfully to improve such diverse problems as incontinence, agitation and aggression (Teri and Gallagher-Thompson, 1991). Although apathy has not been specifically addressed using behavioral interventions to date, evidence suggests that behavioral interventions are effective for treating depression in patients with AD and their caregivers (Teri et al., 1997). Behavioral interventions in dementia have also resulted in improved patient health and lower caregiver burden (Teri et al., 2003). We recently completed a controlled trial of the effectiveness of a novel caregiver-based behavioral training program for reducing apathy in patients with AD and reducing stress among their caregivers. Preliminary findings suggest that behavioral intervention benefited patients with AD and their caregivers (Boyle et al., 2004). Further research examining the benefits of combined, pharmacological-behavioral interventions is needed.
Summary and Conclusions
Apathy is a debilitating and underrecognized syndrome that affects the vast majority of individuals with dementia, results in functional impairment among patients and causes stress among their caregivers. Accurate discrimination of the symptoms of apathy from depression is necessary for optimal treatment. The careful comparison of the symptoms of dysphoria versus symptoms of amotivation is recommended, and a number of instruments have been developed to aid in the discrimination of apathy from depression.
Cholinesterase inhibitors have been shown to reduce the neuropsychiatric symptoms of AD and vascular dementia with apathy showing the most consistent gains. The magnitude and persistence of these changes remains a topic for future research. Traditional antidepressants, activating neurologic agents and combined pharmacological-behavioral treatments also hold promise for the treatment of apathy, but controlled large-scale clinical trials are lacking. For more detailed reviews, the reader is referred to Boyle and Malloy (2004) and Wynn and Cummings (2004).
Dr. Malloy is associate professor at Brown Medical School and co-director of the Butler Hospital Memory Disorders Program.
Dr. Boyle is a neuropsychologist with the Rush Alzheimer's Disease Center and assistant professor in the department of behavioral sciences at Rush University Medical Center.
Source: Paul F. Malloy, Ph.D., and Patricia A. Boyle, Ph.D. Apathy and Its Treatment in Alzheimer's Disease and Other Dementias. Psychiatric Times (2005) Vol. XXIII Issue 13 [FullText, References, and Images]
posted by Dr. Koudinov @ 25.4.06
0 comments
April 19, 2006
Man gets 20-year sentence for sexual assault of Alzheimer's patient
SPARTA, Wis. - A former nurse’s aide who admitted to sexually assaulting a 73-year-old Alzheimer’s patient at a Sparta nursing home in February 2005 will spend 20 years in prison.
Monroe County Circuit Judge Steven Abbott sentenced James Doeslaere, formerly of Bangor, Wis., Tuesday morning to 20 years in a Wisconsin prison and 15 years on extended supervision.
Doeslaere, now 48 and of Camp Douglas, Wis., pleaded guilty Feb. 10 to second-degree sexual assault by a treatment facility employee and intentional abuse of a patient causing bodily harm, both felonies.
Abbott also gave Doeslaere a concurrent sentence of three years in prison and three on extended supervision on the second charge. The charges carried a maximum 46-year sentence.
Doeslaere was a nurse’s aide at Rolling Hills Nursing Home when a co-worker witnessed him straddling an elderly woman in her bed, with her underwear around her ankles, about 2 a.m. Feb 25 in a lockdown ward, according to the criminal complaint.
Doeslaere previously entered a not guilty plea by reason of mental disease. One charge of second-degree sexual assault was dismissed.
Doeslaere originally denied the assault but later admitted it to Monroe County authorities, according to the complaint, telling them he “felt horrible about what he did and he knew that what he did was wrong.”
Though she was teary-eyed and present in court Tuesday, it’s difficult to know whether the woman understood the sentence because her Alzheimer’s disease is in a late stage, Monroe County District Attorney Dan Cary said.
“That’s what makes matters even worse,” Cary said. “It’s a sad case when you put a loved one in trusted care and the trust is violated to this extent.”
Doeslaere was apologetic Tuesday to the victim and the court, Cary said, but showed no emotion when sentenced.
The woman’s husband, 72, said he hoped Doeslaere would receive at least 20 years. “It’s a good feeling when the justice system works in the right way,” he said.
He said his wife still is a patient at Rolling Hills and he visits her three times a day.
He filed a civil lawsuit Oct. 5 in Monroe County Circuit Court against Rolling Hills, administrator Gene Schwarze, Monroe County, Wisconsin County Mutual Insurance Corporation and Doeslaere.
His attorney, Thomas Fitzpatrick, said the nursing home administration should have known Doeslaere was a “dangerous person” because of “prior complaints about him.” A motion hearing for the case is set for 10 a.m. June 28.
Schwarze was not available for comment Tuesday.
Doeslaere will be sent to Dodge Correctional Institution in Waupun, Wis., for processing and assignment to a state prison, Cary said.
He has been free on a $20,000 cash bond since March 2005.
Source: Anne Jungen. Man gets 20-year sentence for sexual assault of Alzheimer's patient. La Crosse Tribune (5 April 2006) [FullText]
Monroe County Circuit Judge Steven Abbott sentenced James Doeslaere, formerly of Bangor, Wis., Tuesday morning to 20 years in a Wisconsin prison and 15 years on extended supervision.
Doeslaere, now 48 and of Camp Douglas, Wis., pleaded guilty Feb. 10 to second-degree sexual assault by a treatment facility employee and intentional abuse of a patient causing bodily harm, both felonies.
Abbott also gave Doeslaere a concurrent sentence of three years in prison and three on extended supervision on the second charge. The charges carried a maximum 46-year sentence.
Doeslaere was a nurse’s aide at Rolling Hills Nursing Home when a co-worker witnessed him straddling an elderly woman in her bed, with her underwear around her ankles, about 2 a.m. Feb 25 in a lockdown ward, according to the criminal complaint.
Doeslaere previously entered a not guilty plea by reason of mental disease. One charge of second-degree sexual assault was dismissed.
Doeslaere originally denied the assault but later admitted it to Monroe County authorities, according to the complaint, telling them he “felt horrible about what he did and he knew that what he did was wrong.”
Though she was teary-eyed and present in court Tuesday, it’s difficult to know whether the woman understood the sentence because her Alzheimer’s disease is in a late stage, Monroe County District Attorney Dan Cary said.
“That’s what makes matters even worse,” Cary said. “It’s a sad case when you put a loved one in trusted care and the trust is violated to this extent.”
Doeslaere was apologetic Tuesday to the victim and the court, Cary said, but showed no emotion when sentenced.
The woman’s husband, 72, said he hoped Doeslaere would receive at least 20 years. “It’s a good feeling when the justice system works in the right way,” he said.
He said his wife still is a patient at Rolling Hills and he visits her three times a day.
He filed a civil lawsuit Oct. 5 in Monroe County Circuit Court against Rolling Hills, administrator Gene Schwarze, Monroe County, Wisconsin County Mutual Insurance Corporation and Doeslaere.
His attorney, Thomas Fitzpatrick, said the nursing home administration should have known Doeslaere was a “dangerous person” because of “prior complaints about him.” A motion hearing for the case is set for 10 a.m. June 28.
Schwarze was not available for comment Tuesday.
Doeslaere will be sent to Dodge Correctional Institution in Waupun, Wis., for processing and assignment to a state prison, Cary said.
He has been free on a $20,000 cash bond since March 2005.
Source: Anne Jungen. Man gets 20-year sentence for sexual assault of Alzheimer's patient. La Crosse Tribune (5 April 2006) [FullText]
posted by Dr. Koudinov @ 19.4.06
0 comments
April 17, 2006
Inside Alzheimer’s
Eighty-six-year-old Evelyn Glover loves looking through her scrapbook. As the pages turn, the people and events that make up her life become familiar once more. Her favorite pictures are those of her daughter, Beth.
"She's been with me all the time when I used to be so wonderful,” Evelyn said with a laugh. “So I sort of went downgrade." Evelyn suffers from Alzheimer's disease. It began with her forgetting little things. Then she couldn't write. Soon she couldn't speak in full sentences.
"It was scary,” Evelyn said. “I didn't know what was happening to me." Then she found Leeza's Place in Melbourne. Leeza's Place is a community outreach center in Brevard County for people with Alzheimer's and their caregivers. It was started by Leeza Gibbons, whose mother and grandmother suffered from the disease.
Evelyn said, "I didn't know what I was going to do or what all this was about and they just took me by hand." "She has to depend on people to feed her and take care of her, and I think that that has really crushed her," Beth Glover said. Soon, she may have to leave her home.
"I wouldn't give up anything for having the place that I have,” Evelyn said. “But they're saying I should go to another and we'll see." As that battle ensues, a little more of Evelyn's memory slips away, forcing her to turn to pictures to remember her life.
Source: Central Florida News 13 (last viewed 7 April 2006) [FullText]
"She's been with me all the time when I used to be so wonderful,” Evelyn said with a laugh. “So I sort of went downgrade." Evelyn suffers from Alzheimer's disease. It began with her forgetting little things. Then she couldn't write. Soon she couldn't speak in full sentences.
"It was scary,” Evelyn said. “I didn't know what was happening to me." Then she found Leeza's Place in Melbourne. Leeza's Place is a community outreach center in Brevard County for people with Alzheimer's and their caregivers. It was started by Leeza Gibbons, whose mother and grandmother suffered from the disease.
Evelyn said, "I didn't know what I was going to do or what all this was about and they just took me by hand." "She has to depend on people to feed her and take care of her, and I think that that has really crushed her," Beth Glover said. Soon, she may have to leave her home.
"I wouldn't give up anything for having the place that I have,” Evelyn said. “But they're saying I should go to another and we'll see." As that battle ensues, a little more of Evelyn's memory slips away, forcing her to turn to pictures to remember her life.
Source: Central Florida News 13 (last viewed 7 April 2006) [FullText]
posted by Dr. Koudinov @ 17.4.06
0 comments
April 15, 2006
Wife's message for Alzheimer's advert
THE words of a wife who is slowly losing her husband to Alzheimer's disease are being featured in a powerful advertising campaign.
Barbara Pointon, 66, has been caring for her husband, Malcolm, 65, at their home in Thriplow for 14 years.
Malcolm and Barbara Pointon Until dementia began to destroy his life, Mr Pointon was a brilliant piano player and music lecturer at Homerton College, Cambridge.
Now the couple's experience is being highlighted in a prime-time television campaign showing the devastating impact of the disease.
"Your brain is what makes you you. But what happens if it goes wrong?" asks Mrs Pointon in the advertisement.
"In the UK today (Monday, 03 April) 750,000 people have Alzheimer's disease or another form of dementia. My husband Malcolm is just one of them.
"It hasn't just switched off his memory. It has systematically shut down his life."
The advertisement, being launched by the Alzheimer's Society, also includes footage of the family and their friends before the illness.
The campaign is currently being shown on digital television channels, but will be shown on terrestrial television before May to tie in with an Alzheimer's storyline in ITV soap Coronation Street.
Mrs Pointon said: "The society has done so much for Malcolm and me, it is the least I could do to help. Without their help I would have gone under and given up a long time ago."
Neil Hunt, chief executive of the Alzheimer's Society, says the adverts are designed to make people think about dementia.
He said: "The death of Malcolm's memories depicted in this advert shows the shattering effect Alzheimer's disease has, not just on the individual but on everyone around them."
The impact of Alzheimer's on the Thriplow couple has previously been featured in a documentary, Malcolm and Barbara: A Love Story, which was voted by Channel 4 viewers as one of the 50 greatest documentaries.
One in 20 people over the age of 65, and one in five over the age of 80, are affected by dementia. More than 18,500 people under the age of 65 in the UK have the disease.
Source: Katherine Pateman. Wife's message for Alzheimer's advert. CEN News (3 April 2006) [FullText]
Barbara Pointon, 66, has been caring for her husband, Malcolm, 65, at their home in Thriplow for 14 years.
Malcolm and Barbara Pointon Until dementia began to destroy his life, Mr Pointon was a brilliant piano player and music lecturer at Homerton College, Cambridge.
Now the couple's experience is being highlighted in a prime-time television campaign showing the devastating impact of the disease.
"Your brain is what makes you you. But what happens if it goes wrong?" asks Mrs Pointon in the advertisement.
"In the UK today (Monday, 03 April) 750,000 people have Alzheimer's disease or another form of dementia. My husband Malcolm is just one of them.
"It hasn't just switched off his memory. It has systematically shut down his life."
The advertisement, being launched by the Alzheimer's Society, also includes footage of the family and their friends before the illness.
The campaign is currently being shown on digital television channels, but will be shown on terrestrial television before May to tie in with an Alzheimer's storyline in ITV soap Coronation Street.
Mrs Pointon said: "The society has done so much for Malcolm and me, it is the least I could do to help. Without their help I would have gone under and given up a long time ago."
Neil Hunt, chief executive of the Alzheimer's Society, says the adverts are designed to make people think about dementia.
He said: "The death of Malcolm's memories depicted in this advert shows the shattering effect Alzheimer's disease has, not just on the individual but on everyone around them."
The impact of Alzheimer's on the Thriplow couple has previously been featured in a documentary, Malcolm and Barbara: A Love Story, which was voted by Channel 4 viewers as one of the 50 greatest documentaries.
One in 20 people over the age of 65, and one in five over the age of 80, are affected by dementia. More than 18,500 people under the age of 65 in the UK have the disease.
Source: Katherine Pateman. Wife's message for Alzheimer's advert. CEN News (3 April 2006) [FullText]
posted by Dr. Koudinov @ 15.4.06
0 comments
April 14, 2006
Alzheimer's hits a century, not out
Treatments for Alzheimer's disease are improving, but experts don't know if progress is fast enough. Ben Sheehan reports
FORGET all those tired old jokes about Alzheimer's, the ones about hiding your own Easter eggs or losing the car keys. Australia is staring down the barrel of an epidemic, exactly 100 years since the disease was discovered.
Alzheimer's does not pose the contagious threat of bird flu, but more Australians are getting it and medicine can't pinpoint a cause.
So where does this leave the baby boomers, the single largest generation in Australia's history, as they trundle forward into old age and the higher risk of developing the disease?
Alzheimer's expert and chairman of the federal Government's Aged Care Committee Mark Yates is not sure. "We don't know how prepared we are (for) an epidemic," he says. "Services are expanding, and the federal Government has made it a national health priority. But we certainly don't know if we'll crack a treatment agent in the near future."
In 2000 there were an estimated 146,800 Australians aged 65 and over who had dementia, according to the Australian Institute of Health and Welfare. Over half of these had Alzheimer's.
But rates have been increasing sharply, a function both of greater recognition of the disease among patients and doctors and also the demographic shifts towards an older population.
According to a report by Access Economics last year, 210,000 Australians of all ages now live with dementia, the majority of whom would have Alzheimer's.
The report, commissioned by Alzheimer's Australia, found there are 1000 new cases every seven days. US data suggests as many as 10 per cent are under 60, a few are even in their 30s. Once you are over 65, there's a one in 50 chance it will be you, and every five years after that your chances of getting it will double.
These and similar statistics are galvanising experts into action. In December experts from the Institute of Psychiatry at King's College, London, called for governments to work together to tackle the disease.
The rationale is simple. Populations are ageing, and few of the available drugs do more than treat symptoms.
Despite the ubiquity of Alzheimer's, it is not considered a part of normal ageing. Theories in the past as to what may cause the disease have included the accumulation in the brain of metals such as aluminium, lead, mercury and other substances, but these notions have now been disproved.
There is no proven way to prevent or cure Alzheimer's, although a study published in The Lancet last week did appear to offer new hope of progress on treatments. The paper (doi:10.1016/S0140-6736(06) 68350-5) was the first to assess the effectiveness of donepezil, a drug already used to treat mild to moderate Alzheimer's, in more severe cases.
The researchers assigned 95 patients with severe Alzheimer's to donepezil – available in Australia under the brand name Aricept – and another 99 to a placebo.
The study, funded by Pfizer, Aricept's maker, found that after six months patients given donepezil had improved cognition and ability to carry out daily tasks. The researchers said the findings showed not only could the drug slow progress of the disease, but could also reverse "some aspects" of mental deterioration.
However, Australian experts have cautioned this falls a long way short of a cure. And there is thus increasing interest in what might we might be able to do to reduce the chances of developing the disease in the first place.
According to Lynette Moore, a member of the federal Government's Dementia Health Priority Task Force, there's a distinct possibility we can stave off the illness through a healthy diet and exercise.
"A growing body of evidence suggests that around mid-life, high cholesterol and blood pressure are associated with Alzheimer's in later life," Moore says. Vascular disease is also regarded as a key risk factor.
Moore believes the evidence so far suggests that avoiding these risk factors and building up more brain cells through mental exercise improves your chances of avoiding Alzheimer's. Yates also thinks that maintaining diversity of thought and activities after retirement might help.
While much remains to be discovered about the causes of Alzheimer's, the best treatments and preventive measures, our ability to diagnose the disease with confidence has improved enormously since Dr Alois Alzheimer in 1906 first described the brain plaques and tangles that have become the hallmarks of the disease.
Catriona McLean, director of the National Neurological Tissue Resource Centre, says while the brain is the only part of the body affected, clinical diagnosis – based on a detailed patient assessment by an experienced specialist, imaging tests and after excluding other possible causes of dementia – can be 80 to 90 per cent accurate.
But the professor says the "only 100 per cent accurate way to make a diagnosis is to examine the brain at autopsy", using tests that mark out the accumulation of abnormal proteins that are characteristic of the disease. McLean, who is also professor of pathology at Monash University and director of the Alfred Hospital's anatomical pathology department, has spent around 90 minutes studying each of hundreds of Alzheimer-affected brains at the centre.
"Because we are still unsure about the causes of the disease, we still need to use human brains to do the relevant research," she says. "It's important for people to understand that some of the advances that have been made have been possible through people who have donated their brains for research."
She says experts now have a much better understanding of the genetic factors involved in Alzheimer's progression, and how the proteins develop in abnormal ways.
But while many experts, including Yates, say earlier detection is vital there are others who question the need to make a firm diagnosis in the early stages of the disease, at least while the treatment options are so limited. Rod Pearce, chairman of the Australian Medical Association's council of general practice, believes that medical intervention is often pointless.
Total disablement from Alzheimer's is common. While the average lifespan after diagnosis is eight to 10 years, some patients live with the disease for 20 years or more.
"This is GPs responding to the reality of what they can do, and often making that diagnosis isn't going to be helpful," Pearce says. "If a GP picks Alzheimer's up but then can't get access to the treatment the patient needs, then what's the advantage of putting a label on it? It's distressing for all involved."
One source of Pearce's frustration is that GPs are unable to prescribe donezepil, or the other Alzheimer's drugs galantamine (Reminyl) and rivastigmine (Exelon) under current Pharmaceutical Benefits Scheme criteria.
Patients require assessment by a gerontologist or psychiatrist and a six-month trial to demonstrate "noticeable improvement" before their doctor is given the green light to write scripts. "When people need help and the treatment is appropriate, the system puts a lot of barriers in the way," says Pearce.
One of these barriers is cost.
Patients with a concession card can get a month's supply of Aricept, Reminyl or Exelon for $4.70. Without the subsidy, the cost of these drugs escalates to between $160 and $190 per month. Another drug called memantine (Ebixa), which is used in conjunction with any one of the three, costs users an additional $170 per month and is not funded by the PBS.
"The cost of medication means that most people end up waiting for their assessment (to gain the PBS subsidy and start medication)," says Pearce, himself a GP. But not all wait. A survey of 1226 patients last year by Alzheimer's Australia found that 27 per cent of sufferers had paid for the drugs out of their own pockets.
Another concern is that patients are often left to decide for themselves if, and when, they give up their car keys. The prospect of losing the ability to drive appals many patients, and many find it difficult to contemplate such a move; but as the need to surrender the car keys grows, the nature of the disease means patients are less equipped to make the decision to do so. Driving assessments are voluntary and cost $180.
Former federal minister for ageing Julie Bishop concedes that many elderly people find losing a driving licence "a highly traumatic event". "One elderly couple who were both diagnosed with dementia skipped their state, Thelma and Louise-style, rather than give up their licence," she says.
Source: Alzheimer's hits a century, not out. Alzheimers.org.au (1 April 2006) [FullText]
FORGET all those tired old jokes about Alzheimer's, the ones about hiding your own Easter eggs or losing the car keys. Australia is staring down the barrel of an epidemic, exactly 100 years since the disease was discovered.
Alzheimer's does not pose the contagious threat of bird flu, but more Australians are getting it and medicine can't pinpoint a cause.
So where does this leave the baby boomers, the single largest generation in Australia's history, as they trundle forward into old age and the higher risk of developing the disease?
Alzheimer's expert and chairman of the federal Government's Aged Care Committee Mark Yates is not sure. "We don't know how prepared we are (for) an epidemic," he says. "Services are expanding, and the federal Government has made it a national health priority. But we certainly don't know if we'll crack a treatment agent in the near future."
In 2000 there were an estimated 146,800 Australians aged 65 and over who had dementia, according to the Australian Institute of Health and Welfare. Over half of these had Alzheimer's.
But rates have been increasing sharply, a function both of greater recognition of the disease among patients and doctors and also the demographic shifts towards an older population.
According to a report by Access Economics last year, 210,000 Australians of all ages now live with dementia, the majority of whom would have Alzheimer's.
The report, commissioned by Alzheimer's Australia, found there are 1000 new cases every seven days. US data suggests as many as 10 per cent are under 60, a few are even in their 30s. Once you are over 65, there's a one in 50 chance it will be you, and every five years after that your chances of getting it will double.
These and similar statistics are galvanising experts into action. In December experts from the Institute of Psychiatry at King's College, London, called for governments to work together to tackle the disease.
The rationale is simple. Populations are ageing, and few of the available drugs do more than treat symptoms.
Despite the ubiquity of Alzheimer's, it is not considered a part of normal ageing. Theories in the past as to what may cause the disease have included the accumulation in the brain of metals such as aluminium, lead, mercury and other substances, but these notions have now been disproved.
There is no proven way to prevent or cure Alzheimer's, although a study published in The Lancet last week did appear to offer new hope of progress on treatments. The paper (doi:10.1016/S0140-6736(06) 68350-5) was the first to assess the effectiveness of donepezil, a drug already used to treat mild to moderate Alzheimer's, in more severe cases.
The researchers assigned 95 patients with severe Alzheimer's to donepezil – available in Australia under the brand name Aricept – and another 99 to a placebo.
The study, funded by Pfizer, Aricept's maker, found that after six months patients given donepezil had improved cognition and ability to carry out daily tasks. The researchers said the findings showed not only could the drug slow progress of the disease, but could also reverse "some aspects" of mental deterioration.
However, Australian experts have cautioned this falls a long way short of a cure. And there is thus increasing interest in what might we might be able to do to reduce the chances of developing the disease in the first place.
According to Lynette Moore, a member of the federal Government's Dementia Health Priority Task Force, there's a distinct possibility we can stave off the illness through a healthy diet and exercise.
"A growing body of evidence suggests that around mid-life, high cholesterol and blood pressure are associated with Alzheimer's in later life," Moore says. Vascular disease is also regarded as a key risk factor.
Moore believes the evidence so far suggests that avoiding these risk factors and building up more brain cells through mental exercise improves your chances of avoiding Alzheimer's. Yates also thinks that maintaining diversity of thought and activities after retirement might help.
While much remains to be discovered about the causes of Alzheimer's, the best treatments and preventive measures, our ability to diagnose the disease with confidence has improved enormously since Dr Alois Alzheimer in 1906 first described the brain plaques and tangles that have become the hallmarks of the disease.
Catriona McLean, director of the National Neurological Tissue Resource Centre, says while the brain is the only part of the body affected, clinical diagnosis – based on a detailed patient assessment by an experienced specialist, imaging tests and after excluding other possible causes of dementia – can be 80 to 90 per cent accurate.
But the professor says the "only 100 per cent accurate way to make a diagnosis is to examine the brain at autopsy", using tests that mark out the accumulation of abnormal proteins that are characteristic of the disease. McLean, who is also professor of pathology at Monash University and director of the Alfred Hospital's anatomical pathology department, has spent around 90 minutes studying each of hundreds of Alzheimer-affected brains at the centre.
"Because we are still unsure about the causes of the disease, we still need to use human brains to do the relevant research," she says. "It's important for people to understand that some of the advances that have been made have been possible through people who have donated their brains for research."
She says experts now have a much better understanding of the genetic factors involved in Alzheimer's progression, and how the proteins develop in abnormal ways.
But while many experts, including Yates, say earlier detection is vital there are others who question the need to make a firm diagnosis in the early stages of the disease, at least while the treatment options are so limited. Rod Pearce, chairman of the Australian Medical Association's council of general practice, believes that medical intervention is often pointless.
Total disablement from Alzheimer's is common. While the average lifespan after diagnosis is eight to 10 years, some patients live with the disease for 20 years or more.
"This is GPs responding to the reality of what they can do, and often making that diagnosis isn't going to be helpful," Pearce says. "If a GP picks Alzheimer's up but then can't get access to the treatment the patient needs, then what's the advantage of putting a label on it? It's distressing for all involved."
One source of Pearce's frustration is that GPs are unable to prescribe donezepil, or the other Alzheimer's drugs galantamine (Reminyl) and rivastigmine (Exelon) under current Pharmaceutical Benefits Scheme criteria.
Patients require assessment by a gerontologist or psychiatrist and a six-month trial to demonstrate "noticeable improvement" before their doctor is given the green light to write scripts. "When people need help and the treatment is appropriate, the system puts a lot of barriers in the way," says Pearce.
One of these barriers is cost.
Patients with a concession card can get a month's supply of Aricept, Reminyl or Exelon for $4.70. Without the subsidy, the cost of these drugs escalates to between $160 and $190 per month. Another drug called memantine (Ebixa), which is used in conjunction with any one of the three, costs users an additional $170 per month and is not funded by the PBS.
"The cost of medication means that most people end up waiting for their assessment (to gain the PBS subsidy and start medication)," says Pearce, himself a GP. But not all wait. A survey of 1226 patients last year by Alzheimer's Australia found that 27 per cent of sufferers had paid for the drugs out of their own pockets.
Another concern is that patients are often left to decide for themselves if, and when, they give up their car keys. The prospect of losing the ability to drive appals many patients, and many find it difficult to contemplate such a move; but as the need to surrender the car keys grows, the nature of the disease means patients are less equipped to make the decision to do so. Driving assessments are voluntary and cost $180.
Former federal minister for ageing Julie Bishop concedes that many elderly people find losing a driving licence "a highly traumatic event". "One elderly couple who were both diagnosed with dementia skipped their state, Thelma and Louise-style, rather than give up their licence," she says.
Source: Alzheimer's hits a century, not out. Alzheimers.org.au (1 April 2006) [FullText]
posted by Dr. Koudinov @ 14.4.06
0 comments
April 13, 2006
Alzheimer's educational series offered in Belmont
BELMONT - The ABC's of Alzheimer's and Dementia is a three-part education series for families of persons diagnosed with Alzheimer's disease or a related dementia. It is designed to enhance your understanding of the disease, how it affects your loved one and how to effectively deal with it day-to-day. This free series is open to the public. It will be held from 6:30 to 8:45 p.m. Wednesdays, April 12, 19 and 26, at the Belmont AmeriHost Inn and Convention Center, Wisconsin 151, exit 26.
On April 12, Dr. Mark Sager of the Wisconsin Alzheimer's Institute will provide an overview of Alzheimer's and other dementias from a medical perspective. Topics will include the effects of dementia on the brain, various causes of dementia, stages and symptoms of Alzheimer's disease, treatment options, and current research.
The April 19 presentation will examine the effects of dementia on the person and offer practical tips and techniques that family and friends can use to decrease confusion and foster success for their loved one who has dementia. Patricia Wilson and Deanna Truedson of the Alzheimer's Association South Central Wisconsin Chapter will provide insights into understanding the causes of difficult behaviors and how to prevent or respond to them through effective communication, structure and routine, activity and involvement, and safety measures.
The final session on April 26 will focus on the special challenges faced by family caregivers and the resources available to them. An experienced family caregiver, Dale Bruhnk, along with Alzheimer's Association Program Director Mary Reines, will discuss the caregiver's journey, how to cope and thrive as a caregiver, how to involve family and friends, and how to access available resources.
Light refreshments and a different packet of resource materials will be provided at each session. The series is free, but donations are welcomed. Space is limited. More information or to register for the series is available by calling the Alzheimer's Association at (800) 272-3900 or (608) 232-3400.
Source: Alzheimer's series offered in Belmont. The Times Plus (4 April 2006) [FullText]
On April 12, Dr. Mark Sager of the Wisconsin Alzheimer's Institute will provide an overview of Alzheimer's and other dementias from a medical perspective. Topics will include the effects of dementia on the brain, various causes of dementia, stages and symptoms of Alzheimer's disease, treatment options, and current research.
The April 19 presentation will examine the effects of dementia on the person and offer practical tips and techniques that family and friends can use to decrease confusion and foster success for their loved one who has dementia. Patricia Wilson and Deanna Truedson of the Alzheimer's Association South Central Wisconsin Chapter will provide insights into understanding the causes of difficult behaviors and how to prevent or respond to them through effective communication, structure and routine, activity and involvement, and safety measures.
The final session on April 26 will focus on the special challenges faced by family caregivers and the resources available to them. An experienced family caregiver, Dale Bruhnk, along with Alzheimer's Association Program Director Mary Reines, will discuss the caregiver's journey, how to cope and thrive as a caregiver, how to involve family and friends, and how to access available resources.
Light refreshments and a different packet of resource materials will be provided at each session. The series is free, but donations are welcomed. Space is limited. More information or to register for the series is available by calling the Alzheimer's Association at (800) 272-3900 or (608) 232-3400.
Source: Alzheimer's series offered in Belmont. The Times Plus (4 April 2006) [FullText]
posted by Dr. Koudinov @ 13.4.06
0 comments
April 12, 2006
Antibody fights Alzheimer's, Rosenberg says
Doses of DNA-gene-coated gold particles protect mice against a protein implicated in Alzheimer's disease, researchers at the University of Texas Southwestern Medical Center have found.
By pressure-injecting the gene responsible for producing the specific protein - called amyloid-beta 42 - the researchers caused the mice to make antibodies and greatly reduce the protein's buildup in the brain. Accumulation of amyloid-beta 42 in humans is a hallmark of Alzheimer's disease.
"The whole point of the study is to determine whether the antibody is therapeutically effective as a means to inhibit the formation of amyloid-beta storage in the brain, and it is," said Roger Rosenberg, M.D., the study's senior author and director of the Alzheimer's Disease Center at UT Southwestern.
The gene injection avoids a serious side effect that caused the cancellation of a previous multicenter human trial with amyloid-beta 42, researchers said. UT Southwestern did not participate in that trial. In that earlier study, people received injections of the protein itself and some developed dangerous brain inflammation.
The new study is available online and appears in an upcoming issue of the Journal of the Neurological Sciences.
The researchers used mutant mice with two defective human genes associated with Alzheimer's that produce amyloid-beta 42. "By seven months, the mice are storing abundant amounts of amyloid-beta 42," Rosenberg said.
While the mice were young, the scientists coated microscopically small gold particles with human amyloid-beta 42 genes attached to other genes that program cells to make the protein. The particles were then injected with a gene gun into the skin cells of the mice's ears using a blast of helium.
After receiving 11 injections over several months, the mice showed a high level of antibodies to amyloid-beta 42 and a 60- percent to 77.5-percent reduction of plaques in their brains.
As controls, the researchers also either injected mutant mice with the gene for a related but harmless protein, amyloid-beta 16, or with a gene vaccine that lacked any amyloid genes. These treatments did not cause antibody production, and the mice showed the large amounts of amyloid-beta 42 brain plaques normally seen in animals with these mutations.
The gene injection showed superior results compared to a previous human study in which amyloid-beta 42 protein itself was injected into muscle, Rosenberg said. That study was halted when a small percentage of participants developed inflammation of the brain and spinal cord.
Injecting the gene, in contrast, caused no brain inflammation in the mice.
Rosenberg said the difference was partly because in the human trial, the protein was injected along with a substance called an adjuvant, which increased the immune response to abnormal excessive levels, causing the dangerous brain inflammation.
In addition, the immune response in humans may have involved antibodies called Th1, which were probably partly responsible for the inflammation. The gene injection in the mouse study produced Th2 antibodies, which have a low probability of causing brain inflammation. Furthermore, no adjuvant was needed for antibody production.
The gene immunization is now undergoing further animal studies, with the ultimate goal being a clinical trial in humans. The researchers also plan to see if it can reverse the size of established plaques in the brains of mice.
This information was provided by the University of Texas Southwestern Medical Center.
Source: myDNA News (3 April 2006) [FullText]
By pressure-injecting the gene responsible for producing the specific protein - called amyloid-beta 42 - the researchers caused the mice to make antibodies and greatly reduce the protein's buildup in the brain. Accumulation of amyloid-beta 42 in humans is a hallmark of Alzheimer's disease.
"The whole point of the study is to determine whether the antibody is therapeutically effective as a means to inhibit the formation of amyloid-beta storage in the brain, and it is," said Roger Rosenberg, M.D., the study's senior author and director of the Alzheimer's Disease Center at UT Southwestern.
The gene injection avoids a serious side effect that caused the cancellation of a previous multicenter human trial with amyloid-beta 42, researchers said. UT Southwestern did not participate in that trial. In that earlier study, people received injections of the protein itself and some developed dangerous brain inflammation.
The new study is available online and appears in an upcoming issue of the Journal of the Neurological Sciences.
The researchers used mutant mice with two defective human genes associated with Alzheimer's that produce amyloid-beta 42. "By seven months, the mice are storing abundant amounts of amyloid-beta 42," Rosenberg said.
While the mice were young, the scientists coated microscopically small gold particles with human amyloid-beta 42 genes attached to other genes that program cells to make the protein. The particles were then injected with a gene gun into the skin cells of the mice's ears using a blast of helium.
After receiving 11 injections over several months, the mice showed a high level of antibodies to amyloid-beta 42 and a 60- percent to 77.5-percent reduction of plaques in their brains.
As controls, the researchers also either injected mutant mice with the gene for a related but harmless protein, amyloid-beta 16, or with a gene vaccine that lacked any amyloid genes. These treatments did not cause antibody production, and the mice showed the large amounts of amyloid-beta 42 brain plaques normally seen in animals with these mutations.
The gene injection showed superior results compared to a previous human study in which amyloid-beta 42 protein itself was injected into muscle, Rosenberg said. That study was halted when a small percentage of participants developed inflammation of the brain and spinal cord.
Injecting the gene, in contrast, caused no brain inflammation in the mice.
Rosenberg said the difference was partly because in the human trial, the protein was injected along with a substance called an adjuvant, which increased the immune response to abnormal excessive levels, causing the dangerous brain inflammation.
In addition, the immune response in humans may have involved antibodies called Th1, which were probably partly responsible for the inflammation. The gene injection in the mouse study produced Th2 antibodies, which have a low probability of causing brain inflammation. Furthermore, no adjuvant was needed for antibody production.
The gene immunization is now undergoing further animal studies, with the ultimate goal being a clinical trial in humans. The researchers also plan to see if it can reverse the size of established plaques in the brains of mice.
This information was provided by the University of Texas Southwestern Medical Center.
Source: myDNA News (3 April 2006) [FullText]
posted by Dr. Koudinov @ 12.4.06
0 comments
April 11, 2006
Canadian astronaut Roberta Bondar: Alzheimer's Mission Launched
Former Canadian astronaut Roberta Bondar is crossing a new frontier with another mission.
Canada's first woman in space and the world's first neurologist astronaut is lending her name to support a national Alzheimer's disease awareness program named Mission for Memories.
"I'm striving to share the knowledge and the insight that I've gained in neurology," said Bondar, who is hosting a public forum on the debilitating disease at the Douglas Hospital in Montreal tonight with an emphasis on early diagnosis and treatment.
"There are medications out there to help. There is no cure but there's hope that there will be some day," Bondar said.
When Bondar completed her post-graduate thesis on Alois Alzheimer and his early research, the brain was an inaccessible frontier.
"When I went into medicine the CT scan had just come out. Up until that time, the brain was in a black box. The only way to get at it was indirectly, either by doing an autopsy or doing surgery - taking a piece of tissue out.
"So we have come a long way since then. We can now put patients in functional MRIs (magnetic resonance imaging machines) and see where the hotspots are. These are incredible leaps."
Alzheimer's is a progressive degenerative disease that causes tangles and plaques in the brain. The disease is characterized by a decline in memory and mental abilities. An estimated 420,000 Canadians age 65 and older have Alzheimer's or a related dementia.
Early diagnoses and treatment of Alzheimer's can help stave off the symptomatic progression of the disease, but only continued research will find the causes and a cure, Bondar said.
There are many advances on the horizon, she said.
"We've found certain cells inside the brain - hidden cells that can rejuvenate - and that we are looking at to try to maybe implant in people with memory loss and other neurologic diseases," she said. "It's very exciting. This is something we didn't know about 10 years ago."
This year marks the 100th anniversary of the identification of Alzheimer's disease.
Bondar's visit to Montreal is the second in a series of public forums planned in six cities across Canada to mark the milestone and highlight important treatment advances.
"It's more exciting now than 30 years ago when I was studying it because of the advances in technology and the fact that the international community is involved," she said.
Douglas researchers recently found that consumption of black and green tea may reduce the risk of age-related degenerative disease. It's among several studies in recent years to tout the benefits of tea.
A Japanese study concluded that drinking tea lowers the prevalence of cognitive impairment. Published last month, the study, which analyzed more than 1,000 Japanese subjects age 70 or older, revealed that people who drank more than two cups of green tea per day had a 50 per cent lower chance of having cognitive impairment compared with those who drank less than three cups per week.
The Quebec forum will be held tonight between 6:30 and 8:30 p.m. at the Douglas Hospital, 6875 LaSalle Blvd., in Verdun. Admission is free.
Source: Charlie Fidelman. Launching into Alzheimer's territory. The Gazette (4 April 2006) [FullText]
Canada's first woman in space and the world's first neurologist astronaut is lending her name to support a national Alzheimer's disease awareness program named Mission for Memories.
"I'm striving to share the knowledge and the insight that I've gained in neurology," said Bondar, who is hosting a public forum on the debilitating disease at the Douglas Hospital in Montreal tonight with an emphasis on early diagnosis and treatment.
"There are medications out there to help. There is no cure but there's hope that there will be some day," Bondar said.
When Bondar completed her post-graduate thesis on Alois Alzheimer and his early research, the brain was an inaccessible frontier.
"When I went into medicine the CT scan had just come out. Up until that time, the brain was in a black box. The only way to get at it was indirectly, either by doing an autopsy or doing surgery - taking a piece of tissue out.
"So we have come a long way since then. We can now put patients in functional MRIs (magnetic resonance imaging machines) and see where the hotspots are. These are incredible leaps."
Alzheimer's is a progressive degenerative disease that causes tangles and plaques in the brain. The disease is characterized by a decline in memory and mental abilities. An estimated 420,000 Canadians age 65 and older have Alzheimer's or a related dementia.
Early diagnoses and treatment of Alzheimer's can help stave off the symptomatic progression of the disease, but only continued research will find the causes and a cure, Bondar said.
There are many advances on the horizon, she said.
"We've found certain cells inside the brain - hidden cells that can rejuvenate - and that we are looking at to try to maybe implant in people with memory loss and other neurologic diseases," she said. "It's very exciting. This is something we didn't know about 10 years ago."
This year marks the 100th anniversary of the identification of Alzheimer's disease.
Bondar's visit to Montreal is the second in a series of public forums planned in six cities across Canada to mark the milestone and highlight important treatment advances.
"It's more exciting now than 30 years ago when I was studying it because of the advances in technology and the fact that the international community is involved," she said.
Douglas researchers recently found that consumption of black and green tea may reduce the risk of age-related degenerative disease. It's among several studies in recent years to tout the benefits of tea.
A Japanese study concluded that drinking tea lowers the prevalence of cognitive impairment. Published last month, the study, which analyzed more than 1,000 Japanese subjects age 70 or older, revealed that people who drank more than two cups of green tea per day had a 50 per cent lower chance of having cognitive impairment compared with those who drank less than three cups per week.
The Quebec forum will be held tonight between 6:30 and 8:30 p.m. at the Douglas Hospital, 6875 LaSalle Blvd., in Verdun. Admission is free.
Source: Charlie Fidelman. Launching into Alzheimer's territory. The Gazette (4 April 2006) [FullText]
posted by Dr. Koudinov @ 11.4.06
0 comments
April 10, 2006
Daughter Helps Mom Get Treatment for Disease with Symptoms Similar to Alzheimer's Disease
About 375,000 people have NPH, a condition that often mimics the symptoms of Alzheimer's or Parkinson's disease
Thirty-six-year-old Debbie Roll had taken her 70-year-old mother from doctor to doctor trying desperately to get a diagnosis to explain the rapid decline in her mother's health.
Within about a year, Roll's mother, Edythe Magduff, went from an independent, financially savvy woman to one who needed round-the-clock nursing and a wheelchair to get around. She had trouble focusing. She became incontinent. And she was falling down several times a day. It became so bad that Roll and her sisters agreed that if their mother showed no signs of improvement they would move her into a nursing home.
Then, one morning, Roll just happened to be watching a network morning show, and everything changed. A neurosurgeon and former patient were being interviewed about normal pressure hydrocephalus (NPH), a condition that often mimics the symptoms of Alzheimer's disease. It was as though they were talking about Roll's mother.
What Is NPH? NPH is an accumulation of excess fluid around the brain. Its three primary symptoms - walking or shuffling the feet as if they're glued to the ground, urinary incontinence and dementia - closely mirror symptoms associated with more commonly diagnosed diseases such as Alzheimer's and Parkinson's. As a result, many people who have NPH do not know they have it or are diagnosed with other diseases.
How Is NPH Diagnosed? People who have the three primary symptoms of NPH should see a neurologist for a complete neurological workup. The exam includes a clinical assessment, CT and/or MRI scans, and other kinds of neurological tests.
How Is NPH Treated? NPH is treated with a shunt. This tube-like device is implanted in the head to drain excess fluid from the brain to the abdomen, where it can be safely absorbed.
What Is The Prognosis For Those Who Have NPH? The prognosis depends on many factors, but cases successfully managed with a shunt can result in a reversal of symptoms. Only a specialist can properly diagnose NPH. Surgery is not for everyone. There are potential risks and complications. Recovery may take time.
How Did Things Turn Out For Roll And Her Mother? Within a month of Roll's seeing that morning show, Magduff got an MRI and was diagnosed with NPH. She was treated with a programmable shunt, and within 48 hours of surgery, Magduff was thinking clearly again. Within several days, she no longer needed a wheelchair, and her incontinence was eliminated. Today, she lives an active life and is grateful to have regained her independence. Roll and her sisters are thrilled to have their mom back.
Source: Hispanic PR Wire Contexto Latino (last viewed 5 April 2006) [FullText]
Thirty-six-year-old Debbie Roll had taken her 70-year-old mother from doctor to doctor trying desperately to get a diagnosis to explain the rapid decline in her mother's health.
Within about a year, Roll's mother, Edythe Magduff, went from an independent, financially savvy woman to one who needed round-the-clock nursing and a wheelchair to get around. She had trouble focusing. She became incontinent. And she was falling down several times a day. It became so bad that Roll and her sisters agreed that if their mother showed no signs of improvement they would move her into a nursing home.
Then, one morning, Roll just happened to be watching a network morning show, and everything changed. A neurosurgeon and former patient were being interviewed about normal pressure hydrocephalus (NPH), a condition that often mimics the symptoms of Alzheimer's disease. It was as though they were talking about Roll's mother.
What Is NPH? NPH is an accumulation of excess fluid around the brain. Its three primary symptoms - walking or shuffling the feet as if they're glued to the ground, urinary incontinence and dementia - closely mirror symptoms associated with more commonly diagnosed diseases such as Alzheimer's and Parkinson's. As a result, many people who have NPH do not know they have it or are diagnosed with other diseases.
How Is NPH Diagnosed? People who have the three primary symptoms of NPH should see a neurologist for a complete neurological workup. The exam includes a clinical assessment, CT and/or MRI scans, and other kinds of neurological tests.
How Is NPH Treated? NPH is treated with a shunt. This tube-like device is implanted in the head to drain excess fluid from the brain to the abdomen, where it can be safely absorbed.
What Is The Prognosis For Those Who Have NPH? The prognosis depends on many factors, but cases successfully managed with a shunt can result in a reversal of symptoms. Only a specialist can properly diagnose NPH. Surgery is not for everyone. There are potential risks and complications. Recovery may take time.
How Did Things Turn Out For Roll And Her Mother? Within a month of Roll's seeing that morning show, Magduff got an MRI and was diagnosed with NPH. She was treated with a programmable shunt, and within 48 hours of surgery, Magduff was thinking clearly again. Within several days, she no longer needed a wheelchair, and her incontinence was eliminated. Today, she lives an active life and is grateful to have regained her independence. Roll and her sisters are thrilled to have their mom back.
Source: Hispanic PR Wire Contexto Latino (last viewed 5 April 2006) [FullText]
posted by Dr. Koudinov @ 10.4.06
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April 09, 2006
Mild Cognitive Impairment Prevalent in Elderly Population; Risk Increases as Age Goes Up and Years of Education Go Down
ROCHESTER, Minn. - (4 April 2006) - Mayo Clinic researchers have found that mild cognitive impairment, a disorder considered a strong early predictor of Alzheimer's disease, is prevalent among the elderly and increases with age and fewer years of education.
Findings from this study, funded by the National Institute on Aging, will be presented Tuesday, April 4, at the American Academy of Neurology meeting in San Diego. The researchers randomly selected 3,957 people from the general population of Olmsted County, Minn., home of Mayo Clinic, for participation in this study. The researchers set out to find how many of those who did not have dementia might have mild cognitive impairment. To date, 1,116 people without dementia in the study have been evaluated.
The findings suggest that 12 percent of 70- to 89-year-olds in Olmsted County, Minn., have mild cognitive impairment. The prevalence of mild cognitive impairment increased with age, affecting 9 percent of those 70 to 79 and nearly 18 percent of those 80 to 89. The prevalence of mild cognitive impairment also varied according to years of education, ranging from 25 percent in those with up to eight years of education, 14 percent in those with nine to 12 years, 9 percent in those with 13 to 16 years, and 8.5 percent in those with greater than 16 years.
The researchers suggest that the increase of mild cognitive impairment with age found in this study parallels the risk elevation with age seen in previous studies of Alzheimer's disease.
"This means that 12 percent to 20 percent of the entire population of those over age 70 may have either mild cognitive impairment or dementia, which is quite significant,"says Ronald Petersen, M.D., Ph.D., Mayo Clinic neurologist and study investigator. "These data have major implications for the future of the health care system and the aging of America."
Dr. Petersen adds that the increased risk for mild cognitive impairment with fewer years of education found in this study parallels other studies'findings of a similar rise in risk for Alzheimer's disease as years of education decrease.
"People with more years of education also may experience a loss of cognitive ability, but they can compensate better and thus they don't demonstrate the symptoms of mild cognitive impairment,"says Rosebud Roberts, M.B.Ch.B., Mayo Clinic epidemiologist and lead study investigator. "It's as though their education protects them from exhibiting the effects of mild cognitive impairment."
Dr. Petersen explains that mild cognitive impairment is " the transitional stage between normal aging and dementia." This condition may encompass deficiencies in any or all of the following categories:
Language -- words don't come as quickly as they once did.
Visuospatial ability -- placement of things in time and space becomes more difficult, such as having trouble getting the proportions right when drawing a box.
Executive function -- decision making becomes more challenging.
Memory -- recent recall diminishes, such as what one did yesterday.
Patients with mild cognitive impairment otherwise function normally in society, indicates Dr. Roberts. In fact, she explains, the symptoms of mild cognitive impairment can be so subtle that they are difficult to detect unless living with the affected person.
The current research findings are preliminary; an additional 800 to 900 people will be evaluated before the study's completion. Mayo Clinic's long-term hope with this research, according to Dr. Roberts, is to identify factors that protect against mild cognitive impairment and help develop treatments for those affected, thus minimizing the likelihood of progression to Alzheimer's disease.
Source: Mayo Clinic. AScribe Newswire (4 April 2006) [FullText]
Findings from this study, funded by the National Institute on Aging, will be presented Tuesday, April 4, at the American Academy of Neurology meeting in San Diego. The researchers randomly selected 3,957 people from the general population of Olmsted County, Minn., home of Mayo Clinic, for participation in this study. The researchers set out to find how many of those who did not have dementia might have mild cognitive impairment. To date, 1,116 people without dementia in the study have been evaluated.
The findings suggest that 12 percent of 70- to 89-year-olds in Olmsted County, Minn., have mild cognitive impairment. The prevalence of mild cognitive impairment increased with age, affecting 9 percent of those 70 to 79 and nearly 18 percent of those 80 to 89. The prevalence of mild cognitive impairment also varied according to years of education, ranging from 25 percent in those with up to eight years of education, 14 percent in those with nine to 12 years, 9 percent in those with 13 to 16 years, and 8.5 percent in those with greater than 16 years.
The researchers suggest that the increase of mild cognitive impairment with age found in this study parallels the risk elevation with age seen in previous studies of Alzheimer's disease.
"This means that 12 percent to 20 percent of the entire population of those over age 70 may have either mild cognitive impairment or dementia, which is quite significant,"says Ronald Petersen, M.D., Ph.D., Mayo Clinic neurologist and study investigator. "These data have major implications for the future of the health care system and the aging of America."
Dr. Petersen adds that the increased risk for mild cognitive impairment with fewer years of education found in this study parallels other studies'findings of a similar rise in risk for Alzheimer's disease as years of education decrease.
"People with more years of education also may experience a loss of cognitive ability, but they can compensate better and thus they don't demonstrate the symptoms of mild cognitive impairment,"says Rosebud Roberts, M.B.Ch.B., Mayo Clinic epidemiologist and lead study investigator. "It's as though their education protects them from exhibiting the effects of mild cognitive impairment."
Dr. Petersen explains that mild cognitive impairment is " the transitional stage between normal aging and dementia." This condition may encompass deficiencies in any or all of the following categories:
Language -- words don't come as quickly as they once did.
Visuospatial ability -- placement of things in time and space becomes more difficult, such as having trouble getting the proportions right when drawing a box.
Executive function -- decision making becomes more challenging.
Memory -- recent recall diminishes, such as what one did yesterday.
Patients with mild cognitive impairment otherwise function normally in society, indicates Dr. Roberts. In fact, she explains, the symptoms of mild cognitive impairment can be so subtle that they are difficult to detect unless living with the affected person.
The current research findings are preliminary; an additional 800 to 900 people will be evaluated before the study's completion. Mayo Clinic's long-term hope with this research, according to Dr. Roberts, is to identify factors that protect against mild cognitive impairment and help develop treatments for those affected, thus minimizing the likelihood of progression to Alzheimer's disease.
Source: Mayo Clinic. AScribe Newswire (4 April 2006) [FullText]
posted by Dr. Koudinov @ 9.4.06
0 comments
April 08, 2006
Ashe, Duff, Hyman Win 2006 Potamkin Prize
At the 58th Annual Meeting of the American Academy of Neurology, to be held April 1-8 in San Diego, Karen Ashe, Karen Duff, and Bradley Hyman will receive the $100,000 Potamkin Prize for Research in Pick’s, Alzheimer’s and Related Diseases.
Sometimes called the “Nobel Prize of Neurology,” the Potamkin Prize honors researchers for their work in advancing the understanding of AD and related illnesses.
Karen Hsiao Ashe directs the Center for Memory Research and Care at the University of Minnesota, and for her this Prize comes hard on the heels of a MetLife Award she received earlier this year. The Alzforum covers Ashe’s research into the molecular correlates of AD-related learning and memory deficits closely; for her most recent paper on an oligomeric form of Aβ, see Aβ*56 story and discussion. Ashe is now focusing on characterizing a pre-tangle form of tau that might cause memory deficits.
Karen Duff is at the Center for Dementia Research at the Nathan S. Kline Institute for Psychiatric Research in Orangeburg, which is part of the New York State Office of Mental Health. As has Ashe, Duff has developed several different animal models to study the role of APP/Aβ and of tau in the pathogenesis of AD. Duff has in recent years focused on using these models to test new treatments for neurofibrillary pathology, such as kinase inhibitors and lithium (e.g., Noble et al., 2005), as well as Aβ sequestration approaches.
Brad Hyman is at Massachusetts General Hospital in Charlestown. Though Hyman’s work ranges widely, he is perhaps best known for his early work displaying the damage to the neuronal system that accounts for the behavioral signs of AD, and more recently for his talent in developing clever ways of imaging disease progression in animal models; see Christie et al., 2001). All three scientists collaborate on occasion (see, e.g., Urbanc et al., 2002). Warmest congratulations to the two Karens and Brad!
Funded by the philanthropic Potamkin Foundation, the prize last year went to John Morris at Washington University, St. Louis, Missouri, and Ronald Petersen at the Mayo Clinic College of Medicine in Rochester, Minnesota, for their work on early diagnosis of AD.—Gabrielle Strobel, adapted from press releases.
Source: AlzForum.Org News (28 March 2006) [FullText]
Sometimes called the “Nobel Prize of Neurology,” the Potamkin Prize honors researchers for their work in advancing the understanding of AD and related illnesses.
Karen Hsiao Ashe directs the Center for Memory Research and Care at the University of Minnesota, and for her this Prize comes hard on the heels of a MetLife Award she received earlier this year. The Alzforum covers Ashe’s research into the molecular correlates of AD-related learning and memory deficits closely; for her most recent paper on an oligomeric form of Aβ, see Aβ*56 story and discussion. Ashe is now focusing on characterizing a pre-tangle form of tau that might cause memory deficits.
Karen Duff is at the Center for Dementia Research at the Nathan S. Kline Institute for Psychiatric Research in Orangeburg, which is part of the New York State Office of Mental Health. As has Ashe, Duff has developed several different animal models to study the role of APP/Aβ and of tau in the pathogenesis of AD. Duff has in recent years focused on using these models to test new treatments for neurofibrillary pathology, such as kinase inhibitors and lithium (e.g., Noble et al., 2005), as well as Aβ sequestration approaches.
Brad Hyman is at Massachusetts General Hospital in Charlestown. Though Hyman’s work ranges widely, he is perhaps best known for his early work displaying the damage to the neuronal system that accounts for the behavioral signs of AD, and more recently for his talent in developing clever ways of imaging disease progression in animal models; see Christie et al., 2001). All three scientists collaborate on occasion (see, e.g., Urbanc et al., 2002). Warmest congratulations to the two Karens and Brad!
Funded by the philanthropic Potamkin Foundation, the prize last year went to John Morris at Washington University, St. Louis, Missouri, and Ronald Petersen at the Mayo Clinic College of Medicine in Rochester, Minnesota, for their work on early diagnosis of AD.—Gabrielle Strobel, adapted from press releases.
Source: AlzForum.Org News (28 March 2006) [FullText]
posted by Dr. Koudinov @ 8.4.06
0 comments
April 07, 2006
Street star backed dementia campaign
TV's Coronation Street star Johnny Briggs is backing a campaign with the Alzheimer's Society following his soap character's descent into dementia. The actor is helping with a fundraising appeal to aid those affected by the disease.
Street fans have seen the Weatherfield factory boss Mike Baldwin's mental and physical health deteriorate in the last few months as he battles Alzheimer's. In a direct mail campaign, beginning today, Briggs, 70, whose final scenes after 30 years in the soap are broadcast on Friday, asks donors to support the society's work.
'Walk away'
The star said: "I was lucky when the director said 'cut' I could walk away from Alzheimer's disease.
"Thousands can't. To see someone like Mike affected by Alzheimer's does bring it home that it is not just older people who develop this dreadful illness and it isn't just the person with dementia who is affected, it's everyone around them too."
The society's fundraising director Jo Swinhoe said: "The latest Coronation Street storyline demonstrates that dementia can affect every street in the country, yet people with dementia and their families are not getting the care and support they need, and we still have so much to learn in our search for a cure."
Source: Daily Mail (5 April 2006) [FullText]
Street fans have seen the Weatherfield factory boss Mike Baldwin's mental and physical health deteriorate in the last few months as he battles Alzheimer's. In a direct mail campaign, beginning today, Briggs, 70, whose final scenes after 30 years in the soap are broadcast on Friday, asks donors to support the society's work.
'Walk away'
The star said: "I was lucky when the director said 'cut' I could walk away from Alzheimer's disease.
"Thousands can't. To see someone like Mike affected by Alzheimer's does bring it home that it is not just older people who develop this dreadful illness and it isn't just the person with dementia who is affected, it's everyone around them too."
The society's fundraising director Jo Swinhoe said: "The latest Coronation Street storyline demonstrates that dementia can affect every street in the country, yet people with dementia and their families are not getting the care and support they need, and we still have so much to learn in our search for a cure."
Source: Daily Mail (5 April 2006) [FullText]
posted by Dr. Koudinov @ 7.4.06
0 comments
April 06, 2006
Genetic factors important in development and timing of Alzheimer's disease
A large study of twins, published in the Archives of General Psychiatry, found that Alzheimer's disease appears to be highly heritable and genetic factors may also influence timing of the disease.
Two-thirds of adults aged 65 years and older with dementia have Alzheimer's disease, and the number of Alzheimer's disease cases is predicted to increase with the growing older adult population.
Although genetic risk factors for Alzheimer's disease have been identified, only a fraction of Alzheimer's disease cases can be explained by specific gene mutations. Studies of twins have been helpful in investigating the relative importance of genetic and environmental influences in disease development. For example, if monozygotic twins do not both have a disease, environmental factors may be implicated for its occurrence.
Margaret Gatz, at the University of Southern California, Los Angeles, and colleagues evaluated 11,884 pairs of twins from the Swedish Twin Registry to examine the association between genetic and environmental influences and Alzheimer's disease. The study included patients from the registry who tested positive for dementia and their twins, plus a sample of twins without dementia. The researchers identified 392 pairs of twins in which one or both had Alzheimer's disease.
The researchers estimated heritability for Alzheimer's disease to be between 58 and 79 percent. Among pairs where both twins had Alzheimer's disease, there was an average of 3.66 years difference in age at onset between 25 sets of identical twins, and 8.12 years difference between 20 sets of dizygotic twins.
This lead the researchers to conclude that genes had a role in disease timing "…because age at onset of Alzheimer's disease is significantly more similar for concordant monozygotic pairs compared with concordant dizygotic pairs." Concordance rates were higher in women, reflecting their greater longevity.
" In the largest twin study to date, we confirmed that heritability for Alzheimer's disease is high and that the same genetic factors are influential for both men and women," the authors write. " However, nongenetic risk factors also play an important role and might be the focus for interventions to reduce disease risk or delay disease onset."
Source: American Medical Association, 2006, XagenaMedicine2006 (last viewed 6 April 2006) [FullText]
Two-thirds of adults aged 65 years and older with dementia have Alzheimer's disease, and the number of Alzheimer's disease cases is predicted to increase with the growing older adult population.
Although genetic risk factors for Alzheimer's disease have been identified, only a fraction of Alzheimer's disease cases can be explained by specific gene mutations. Studies of twins have been helpful in investigating the relative importance of genetic and environmental influences in disease development. For example, if monozygotic twins do not both have a disease, environmental factors may be implicated for its occurrence.
Margaret Gatz, at the University of Southern California, Los Angeles, and colleagues evaluated 11,884 pairs of twins from the Swedish Twin Registry to examine the association between genetic and environmental influences and Alzheimer's disease. The study included patients from the registry who tested positive for dementia and their twins, plus a sample of twins without dementia. The researchers identified 392 pairs of twins in which one or both had Alzheimer's disease.
The researchers estimated heritability for Alzheimer's disease to be between 58 and 79 percent. Among pairs where both twins had Alzheimer's disease, there was an average of 3.66 years difference in age at onset between 25 sets of identical twins, and 8.12 years difference between 20 sets of dizygotic twins.
This lead the researchers to conclude that genes had a role in disease timing "…because age at onset of Alzheimer's disease is significantly more similar for concordant monozygotic pairs compared with concordant dizygotic pairs." Concordance rates were higher in women, reflecting their greater longevity.
" In the largest twin study to date, we confirmed that heritability for Alzheimer's disease is high and that the same genetic factors are influential for both men and women," the authors write. " However, nongenetic risk factors also play an important role and might be the focus for interventions to reduce disease risk or delay disease onset."
Source: American Medical Association, 2006, XagenaMedicine2006 (last viewed 6 April 2006) [FullText]
posted by Dr. Koudinov @ 6.4.06
0 comments
April 05, 2006
Two New Drugs for the Treatment of Alzheimer's Disease are Expected to Enter the Market by 2008
DUBLIN, Ireland - (April 4, 2006) - Research and Markets has announced the addition of Emerging Diagnostic Markers in Alzheimers Disease to their offering.
- Currently, the most promising diagnostic agent for Alzheimer's disease (AD) is Pittsburgh Compound B, an A(beta)-amyloid imaging agent in development by GE Healthcare. We expect this agent to reach the market by 2011 and to increase the number of diagnosed and drug-treated patients by 2013.
- Several drugs are in development for treatment of AD; we expect two of these to reach the market by 2008. To be most effective, these treatments must be initiated in patients as soon as possible.
- Besides elucidating the progression of AD, a biomarker for AD would increase drug-treatment rates and therefore increase revenues for drug companies with marketed AD therapies. The increase in drug-treatment rates would result from earlier diagnosis of more patients and, consequently, longer durations of disease treatment. However, if no biomarker becomes available during our study period, we estimate that AD drugs will not attain their full market potential.
- The potential for sales of an AD diagnostic agent could be significant, due to the increasing prevalence of the disease and the potential for a diagnostic agent to command better pricing than a traditional diagnostic, given the large unmet need.
- A diagnostic agent approved by the FDA as an efficacy end point could dramatically grow the market potential for a disease-modifying drug by increasing diagnosis rates, drug-treatment rates, and duration of therapy. A therapeutic agent that demonstrated disease modification based on a biomarker could command a significant premium.
- An AD biomarker will greatly reduce costs associated with drug development by enabling selection of a more homogeneous patient population for smaller, more cost-effective clinical trials. A biomarker will also accelerate drug development by facilitating decisions as to whether to pursue or abandon agents in the early stages of clinical development.
Currently, Alzheimers disease (AD) is diagnosed based on patient clinical history and exclusion of other neurological disorders. Because early signs of AD are hard to distinguish from normal signs of aging, most patients are not diagnosed until neuronal damage is extensive. A diagnostic marker would enable physicians to diagnose more AD patients earlier and begin drug treatment when it could be most effective. The AD therapeutics market would also benefit: early diagnosis and treatment translates to more therapy sales over longer treatment periods.
In this Decision Resources report, we review AD diagnostic markers currently in use and in development, the main players in the AD diagnostics arena, and the impact that these markers will have on the U.S. AD market over the next ten years.
Topics Covered
-- Introduction
-- Pathophysiology of Alzheimers Disease
-- Value of a Biomarker for Alzheimers Disease
-- Necessary Attributes of Alzheimers Disease Biochemical Markers
-- Emerging Imaging Agents for Diagnosis of Alzheimers Disease
-- Key Players in Alzheimers Disease Diagnostics
-- Market Implications
-- Outlook
-- Figure 1. Amyloid Plaques and Neurofibrillary Tangles in Alzheimer's Disease
-- Figure 2. The Bio-Barcode Assay
-- Figure 3. Duration of Therapy for Alzheimer's Disease
-- Figure 4. Potential Sales Scenarios for an Alzheimer's Disease Therapy
-- Figure 5. Major Events the Alzheimer's Disease Market, US
-- Table 1. Current Markers Used in the Diagnosis of Alzheimer's Disease
-- Table 2. Select Companies Pursuing Alzheimer's Disease Diagnostics
-- Table 3. Select Collaborations in Alzheimer's Disease Diagnostics
Companies Mentioned
-- Applied Neurosolutions
-- Aspect Medical Systems
-- AstraZeneca
-- Athena Diagnostics
-- Avid Radiopharmaceuticals
-- BioMerieux
-- Celera Diagnostics
-- deCode Diagnostics
-- Eisai
-- Dyax
-- Innogenetics
-- Kronos Science Laboratories
-- Takeda Chemical Industries
-- Izalex
-- National Institute on Aging (NIA)
-- Perlegen Sciences
-- Pfizer
-- Power3 Medical ProductsProteome Sciences
-- Roche Diagnostics
-- Translational Genomics Research Institute
For more information visit www.researchandmarkets.com
Source: Business Wire (4 April 2006) [FullText]
- Currently, the most promising diagnostic agent for Alzheimer's disease (AD) is Pittsburgh Compound B, an A(beta)-amyloid imaging agent in development by GE Healthcare. We expect this agent to reach the market by 2011 and to increase the number of diagnosed and drug-treated patients by 2013.
- Several drugs are in development for treatment of AD; we expect two of these to reach the market by 2008. To be most effective, these treatments must be initiated in patients as soon as possible.
- Besides elucidating the progression of AD, a biomarker for AD would increase drug-treatment rates and therefore increase revenues for drug companies with marketed AD therapies. The increase in drug-treatment rates would result from earlier diagnosis of more patients and, consequently, longer durations of disease treatment. However, if no biomarker becomes available during our study period, we estimate that AD drugs will not attain their full market potential.
- The potential for sales of an AD diagnostic agent could be significant, due to the increasing prevalence of the disease and the potential for a diagnostic agent to command better pricing than a traditional diagnostic, given the large unmet need.
- A diagnostic agent approved by the FDA as an efficacy end point could dramatically grow the market potential for a disease-modifying drug by increasing diagnosis rates, drug-treatment rates, and duration of therapy. A therapeutic agent that demonstrated disease modification based on a biomarker could command a significant premium.
- An AD biomarker will greatly reduce costs associated with drug development by enabling selection of a more homogeneous patient population for smaller, more cost-effective clinical trials. A biomarker will also accelerate drug development by facilitating decisions as to whether to pursue or abandon agents in the early stages of clinical development.
Currently, Alzheimers disease (AD) is diagnosed based on patient clinical history and exclusion of other neurological disorders. Because early signs of AD are hard to distinguish from normal signs of aging, most patients are not diagnosed until neuronal damage is extensive. A diagnostic marker would enable physicians to diagnose more AD patients earlier and begin drug treatment when it could be most effective. The AD therapeutics market would also benefit: early diagnosis and treatment translates to more therapy sales over longer treatment periods.
In this Decision Resources report, we review AD diagnostic markers currently in use and in development, the main players in the AD diagnostics arena, and the impact that these markers will have on the U.S. AD market over the next ten years.
Topics Covered
-- Introduction
-- Pathophysiology of Alzheimers Disease
-- Value of a Biomarker for Alzheimers Disease
-- Necessary Attributes of Alzheimers Disease Biochemical Markers
-- Emerging Imaging Agents for Diagnosis of Alzheimers Disease
-- Key Players in Alzheimers Disease Diagnostics
-- Market Implications
-- Outlook
-- Figure 1. Amyloid Plaques and Neurofibrillary Tangles in Alzheimer's Disease
-- Figure 2. The Bio-Barcode Assay
-- Figure 3. Duration of Therapy for Alzheimer's Disease
-- Figure 4. Potential Sales Scenarios for an Alzheimer's Disease Therapy
-- Figure 5. Major Events the Alzheimer's Disease Market, US
-- Table 1. Current Markers Used in the Diagnosis of Alzheimer's Disease
-- Table 2. Select Companies Pursuing Alzheimer's Disease Diagnostics
-- Table 3. Select Collaborations in Alzheimer's Disease Diagnostics
Companies Mentioned
-- Applied Neurosolutions
-- Aspect Medical Systems
-- AstraZeneca
-- Athena Diagnostics
-- Avid Radiopharmaceuticals
-- BioMerieux
-- Celera Diagnostics
-- deCode Diagnostics
-- Eisai
-- Dyax
-- Innogenetics
-- Kronos Science Laboratories
-- Takeda Chemical Industries
-- Izalex
-- National Institute on Aging (NIA)
-- Perlegen Sciences
-- Pfizer
-- Power3 Medical ProductsProteome Sciences
-- Roche Diagnostics
-- Translational Genomics Research Institute
For more information visit www.researchandmarkets.com
Source: Business Wire (4 April 2006) [FullText]
posted by Dr. Koudinov @ 5.4.06
0 comments
April 04, 2006
Alzheimer's Patient Missed
FEDERAL WAY, Washington - A man with serious medical problems, including Alzheimer's disease, has been missing since Thursday afternoon, KIRO 7 Eyewitness News Reported.
Ronald Schoeline, 74, disappeared from his Federal Way home around 2 p.m. Thursday.
Searchers looked for Schoeline into Thursday night. "He is not very mobile. He has a limp, rather pronounced from what they describe,” said Search and Rescue Explorer Nick Menyhard. Schoeline was wearing a black leather jacket, khaki pants and a white T-shirt with "Texas" on it.
Searchers want to find the man as soon as possible because they fear he may get hypothermia..."
Source: Man With Alzheimer's Disease Missing. KitoTV.com (31 March 2006) [FullText]
Ronald Schoeline, 74, disappeared from his Federal Way home around 2 p.m. Thursday.
Searchers looked for Schoeline into Thursday night. "He is not very mobile. He has a limp, rather pronounced from what they describe,” said Search and Rescue Explorer Nick Menyhard. Schoeline was wearing a black leather jacket, khaki pants and a white T-shirt with "Texas" on it.
Searchers want to find the man as soon as possible because they fear he may get hypothermia..."
Source: Man With Alzheimer's Disease Missing. KitoTV.com (31 March 2006) [FullText]
posted by Dr. Koudinov @ 4.4.06
0 comments
April 03, 2006
DNA Gene Vaccine Protects Against Harmful Protein of Alzheimer's Disease
Doses of DNA-gene-coated gold particles protect mice against a protein implicated in Alzheimer's disease, researchers at UT Southwestern Medical Center have found.
By pressure-injecting the gene responsible for producing the specific protein - called amyloid-beta 42 - the researchers caused the mice to make antibodies and greatly reduce the protein's build-up in the brain. Accumulation of amyloid-beta 42 in humans is a hallmark of Alzheimer's disease.
"The whole point of the study is to determine whether the antibody is therapeutically effective as a means to inhibit the formation of amyloid-beta storage in the brain, and it is," said Dr. Roger Rosenberg, the study's senior author and director of the Alzheimer's Disease Center at UT Southwestern.
The gene injection avoids a serious side-effect that caused the cancellation of a previous multi-center human trial with amyloid-beta 42, researchers said. UT Southwestern did not participate in that trial. In that earlier study, people received injections of the protein itself and some developed dangerous brain inflammation.
The new study is available online and appears in an upcoming issue of the Journal of the Neurological Sciences.
The researchers used mutant mice with two defective human genes associated with Alzheimer's, genes that produce amyloid-beta 42. "By seven months, the mice are storing abundant amounts of amyloid-beta 42," said Dr. Rosenberg.
While the mice were young, the scientists coated microscopically small gold particles with human amyloid-beta 42 genes attached to other genes that program cells to make the protein. The particles were then injected with a gene gun into the skin cells of the mice's ears using a blast of helium.
After receiving 11 injections over several months, the mice showed a high level of antibodies to amyloid-beta 42, and a 60 percent to 77.5 percent reduction of plaques in their brains.
As controls, the researchers also either injected mutant mice with the gene for a related but harmless protein, amyloid-beta 16, or with a gene vaccine that lacked any amyloid genes. These treatments did not cause antibody production, and the mice showed the large amounts of amyloid-beta 42 brain plaques normally seen in animals with these mutations.
The gene injection showed superior results compared to a previous human study in which amyloid-beta 42 protein itself was injected into muscle, Dr. Rosenberg said. That study was halted when a small percentage of participants developed inflammation of the brain and spinal cord.
Injecting the gene, in contrast, caused no brain inflammation in the mice.
Dr. Rosenberg said the difference was partly because in the human trial, the protein was injected along with a substance called an adjuvant, which increased the immune response to abnormal excessive levels, causing the dangerous brain inflammation. In addition, the immune response in humans may have involved antibodies called Th1, which were probably partly responsible for the inflammation. The gene injection in the mouse study produced Th2 antibodies, which have a low probability of causing brain inflammation. Furthermore, no adjuvant was needed for antibody production.
The gene immunization is now undergoing further animal studies, with the ultimate goal being a clinical trial in humans. The researchers also plan to see if it can reverse the size of established plaques in the brains of mice.
Other UT Southwestern researchers involved in the study were Drs. Bao-Xi Qu, assistant professor of neurology, Philip Boyer, assistant professor of pathology, and Linda Hynan, associate professor of clinical sciences and psychiatry. Dr. Stephen Johnston, formerly with UT Southwestern and now at Arizona State University, also participated.
The work was supported by the National Institute on Aging, the National Alzheimer's Coordinating Center, the Rudman Foundation, the Luttrell Foundation, and UT Southwestern's Winspear Family Special Center for Research on the Neuropathy of Alzheimer's Disease.
Source: Southwestern Medical Center (1 April 2006) [FullText]
By pressure-injecting the gene responsible for producing the specific protein - called amyloid-beta 42 - the researchers caused the mice to make antibodies and greatly reduce the protein's build-up in the brain. Accumulation of amyloid-beta 42 in humans is a hallmark of Alzheimer's disease.
"The whole point of the study is to determine whether the antibody is therapeutically effective as a means to inhibit the formation of amyloid-beta storage in the brain, and it is," said Dr. Roger Rosenberg, the study's senior author and director of the Alzheimer's Disease Center at UT Southwestern.
The gene injection avoids a serious side-effect that caused the cancellation of a previous multi-center human trial with amyloid-beta 42, researchers said. UT Southwestern did not participate in that trial. In that earlier study, people received injections of the protein itself and some developed dangerous brain inflammation.
The new study is available online and appears in an upcoming issue of the Journal of the Neurological Sciences.
The researchers used mutant mice with two defective human genes associated with Alzheimer's, genes that produce amyloid-beta 42. "By seven months, the mice are storing abundant amounts of amyloid-beta 42," said Dr. Rosenberg.
While the mice were young, the scientists coated microscopically small gold particles with human amyloid-beta 42 genes attached to other genes that program cells to make the protein. The particles were then injected with a gene gun into the skin cells of the mice's ears using a blast of helium.
After receiving 11 injections over several months, the mice showed a high level of antibodies to amyloid-beta 42, and a 60 percent to 77.5 percent reduction of plaques in their brains.
As controls, the researchers also either injected mutant mice with the gene for a related but harmless protein, amyloid-beta 16, or with a gene vaccine that lacked any amyloid genes. These treatments did not cause antibody production, and the mice showed the large amounts of amyloid-beta 42 brain plaques normally seen in animals with these mutations.
The gene injection showed superior results compared to a previous human study in which amyloid-beta 42 protein itself was injected into muscle, Dr. Rosenberg said. That study was halted when a small percentage of participants developed inflammation of the brain and spinal cord.
Injecting the gene, in contrast, caused no brain inflammation in the mice.
Dr. Rosenberg said the difference was partly because in the human trial, the protein was injected along with a substance called an adjuvant, which increased the immune response to abnormal excessive levels, causing the dangerous brain inflammation. In addition, the immune response in humans may have involved antibodies called Th1, which were probably partly responsible for the inflammation. The gene injection in the mouse study produced Th2 antibodies, which have a low probability of causing brain inflammation. Furthermore, no adjuvant was needed for antibody production.
The gene immunization is now undergoing further animal studies, with the ultimate goal being a clinical trial in humans. The researchers also plan to see if it can reverse the size of established plaques in the brains of mice.
Other UT Southwestern researchers involved in the study were Drs. Bao-Xi Qu, assistant professor of neurology, Philip Boyer, assistant professor of pathology, and Linda Hynan, associate professor of clinical sciences and psychiatry. Dr. Stephen Johnston, formerly with UT Southwestern and now at Arizona State University, also participated.
The work was supported by the National Institute on Aging, the National Alzheimer's Coordinating Center, the Rudman Foundation, the Luttrell Foundation, and UT Southwestern's Winspear Family Special Center for Research on the Neuropathy of Alzheimer's Disease.
Source: Southwestern Medical Center (1 April 2006) [FullText]
posted by Dr. Koudinov @ 3.4.06
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April 02, 2006
Celebrating 25 years towards finding a cure for Alzheimer's Disease
It was a celebration of life and research progress towards finding a cure for Alzheimer's Disease at the Riverside Convention Center. The local chapter of the Alzheimer's' Association held their annual gala, celebrating 25 years of advances in the quality of life for people with the disease and their caregivers. The event was emceed by New 8 Now's Kevin Doran and featured music from the Rochester Philharmonic Orchestra. RPO conductor Jeff Tyzik says this is his gift after the disease touched his own family."We've all know somebody that's had some person that either family member, relative or somebody they know that's been touched by the disease, and we've been through it in our family," says Tyzik. The event included a silent auction and a gourmet dinner. News 8 Now was a proud sponsor of the event.
Source: WrocTV (2 April 2006) [FullText]
Source: WrocTV (2 April 2006) [FullText]
posted by Dr. Koudinov @ 2.4.06
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April 01, 2006
ISAI, DNAVEC Join in Drug Discovery Research for Alzheimer's Disease
Tokyo (31 March 2006) - Eisai has signed an agreement with DNAVEC on drug discovery research for Alzheimer's disease (AD). Under the agreement, the two companies aim to develop a vaccine therapy for AD.
Specifically, using DNAVEC's proprietary Sendai virus vector, they plan to develop a gene vaccine that can selectively induce the production of anti-beta amyloid antibodies. Beta amyloid is considered to play a role in preventing and suppressing the progress of AD.
Eisai has a prior right to develop, manufacture and sell results obtained from the partnership.
Source: Jcn, JCN Staff Writer JCN (31 March 2006) [FullText]
Specifically, using DNAVEC's proprietary Sendai virus vector, they plan to develop a gene vaccine that can selectively induce the production of anti-beta amyloid antibodies. Beta amyloid is considered to play a role in preventing and suppressing the progress of AD.
Eisai has a prior right to develop, manufacture and sell results obtained from the partnership.
Source: Jcn, JCN Staff Writer JCN (31 March 2006) [FullText]
posted by Dr. Koudinov @ 1.4.06
0 comments
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