Alzheimer's Club

Carl Zeiss MicroImaging, Inc. and Carl Zeiss Surgical, Inc. both based in Thornwood, New York, have made a $100,000 contribution to Barrow Neurological Foundation for use in research projects at Barrow Neurological Institute in Phoenix, Arizona.

Carl Zeiss Surgical, Inc. (CZSI) has a long-standing relationship with St. Joseph's Hospital Barrow Neurological Institute and Robert F. Spetzler, M.D. Chair, Neurological Research. This relationship between Carl Zeiss and Dr. Spetzler was a key driving force in the creation of the OPMI(R) Pentero(TM), the revolutionary surgical microscope platform for neurosurgery, spine surgery and neurotology. In 2004, OPMI Pentero received the International Red-Dot Design Award.

"The OPMI Pentero is unlike any other surgical microscope. In addition to providing premiere quality optics, the OPMI Pentero serves as an information and communication platform, allowing the surgeon to incorporate and utilize various types of information and data from multiple sources," explains Michael Brennan, Neurosurgery Marketing Manager at CZSI.

In addition, Barrow researchers will be collaborating with Zeiss on applications for the company's new PALM Laser Microdissection system, a laser-capture microscope that Barrow recently purchased. Barrow will be the first center in Arizona and one of only a few with the Zeiss PALM system used in neuroscience, the most versatile laser microdissection microscopy system currently available.

The PALM MicroBeam system will allow Barrow researchers to capture and dissect extremely small bits of genetic material such as chromosomes, capture cells from cryopreserved and fixed tissues, and isolate live cells from culture. Barrow scientists will use the PALM system in a wide range of neurological research activities, including research into brain cancer, benign meningiomas, Alzheimer's disease, epilepsy, Parkinson's disease, developmental genetics, multiple sclerosis and Lou Gehrig's disease.

Barrow Neurological Institute is a major academic neuroscience center that is part of St. Joseph's Hospital and Medical Center in Phoenix. Barrow Neurological Foundation raises funds in support of the institute.

Carl Zeiss MicroImaging is a leader in advanced microscopy systems for research, clinical laboratories, and industry. The company offers all types of microscopes and image analysis systems, including the unique LSM 5 LIVE confocal laser scanning microscope for live cell studies, a winner of 2004 R&D 100 Award.

Carl Zeiss is a leading international group of companies operating worldwide in the optical and opto-electronic industry. Carl Zeiss AG is headquartered in Oberkochen, Germany. The Carl Zeiss Group consists of six business units that operate with sole responsibility. They are generally ranked first or second in the three strategic markets of biomedical research and medical technology, system solutions for semiconductor, automotive and mechanical engineering industries, and optical consumer goods such as eyeglass lenses, camera lenses and binoculars. The Carl Zeiss Group is directly represented in more than 30 countries and operates production facilities in Europe, America and Asia. In fiscal year 2004/05 (ended September 30) the Carl Zeiss Group generated revenues totaling EUR 2,222 million. It employs 11,500 people across the globe, including 3,300 outside Germany. The eyeglass business has been merged with the US company Sola International and now operates as Carl Zeiss Vision International GmbH. This company is owned 50:50 by Carl Zeiss AG and a private equity company. Further information is available at www.zeiss.com.

Source: Business Wire (25 January 2006) [FullText]

Results Suggest Alzheimer's Disease May Be More Common than Previously Recognized


A new study from Rush University MedicalCenter helps explain why gait problems are often progressive in old age and related to risk of dementia and death.

The study, published in the January issue of the Annals of Neurology, found that neurofibrillary tangles in the substantia nigra, a part of the brain that is subject to cell loss in Parkinson's disease, are associated with gait impairment in older persons with and without dementia. Neurofibrillary tangles are a classic brain abnormality seen in Alzheimer's disease. The more tangle pathology in the substantia nigra, the more impaired the person's gait was before death.

"Older persons without Parkinson's disease often exhibit parkinsonian signs, such as difficulty with walking and balance (gait impairment), slowness in movements, rigidity and tremor," said study author Dr. Julie Schneider of the Rush Alzheimer's Disease Center. "The mild parkinsonian signs associated with aging have been historically viewed simply as an expected sign of aging rather than a disease process. Previous studies have shown that at least one of these signs, gait impairment, has harmful effects in older persons, and our current study suggests why this may be the case."

The study included 86 autopsied subjects from the Religious Orders Study, a longitudinal clinical-pathological study of aging and dementia. Participants of the Religious Orders Study are older Catholic clergy who enroll without known dementia and agree to annual follow-up and brain donation at death.

The study included persons with and without dementia but excluded people with idiopathic Parkinson's disease. Though less than half of the subjects had dementia, the study found nearly 78 percent of test subjects had neurofibrillary tangles in the substantia nigra. Annual neurological examinations included an assessment of parkinsonian signs using the Unified Parkinson's Disease Rating Scale. All 86 persons had at least some evidence of parkinsonian signs before death. Gait was the most severely affected domain followed by bradykinesia (slowness in movement), rigidity, and tremor.

The study looked at the relationship between nigra tangles and each parkinsonian sign. It found that every 1,000 nigra tangles increased the gait score by more than three points. In contrast, nigra tangles were not related to bradykinesia, rigidity, or tremor. The relationship between substantia nigra tangles and gait impairment was found in persons with and without dementia.

"This study shows that the spectrum of Alzheimer's disease is broader than we thought and may be more common than previously recognized. Alzheimer's disease doesn't just cause memory and cognitive problems, it is also causing motor problems in aging," says Schneider.

"Gait problems in older people should not simply be passed over as a sign of aging. Physicians should be aware that this could be a possible early sign of Alzheimer's disease."

Researchers at Rush continue to study if Alzheimer's disease pathology is impacting other motor regions of the brain and look into whether Alzheimer's disease can only affect motor function without causing cognitive or memory declines. Another study Schneider is currently conducting involves the relationship between dopamine, which is produced in the substantia nigra, and gait changes.

More than 1000 older Catholic clergy from 40 groups across the U.S. are participating in the Religious Orders Study. The study is funded by the National Institute on Aging (NIA).All participants have agreed to annual memory testing and brain donation at the time of death. Schneider and her colleagues at the Rush Alzheimer's Disease Center are grateful for the remarkable dedication and altruism of this unique group of people committed to helping gain insights into how the brain functions with age.

The Rush Alzheimer's Disease Center is one of 29 NIA-supported Alzheimer's Disease Centers across the U.S. which conduct basic science, clinical, and social and behavioral research on dementia and AD. General information on aging and aging research can be viewed at the NIA's home website, www.nia.nih.gov.

Source: Brain Abnormality Found In Alzheimer’s Disease Related to Gait Impairment in Older Persons. Pharma Live (24 January 2006) [FullText]

Meth users can have serious health problems, including having symptoms similar to Parkinson's and Alzheimer's disease.

Methamphetamine is an addictive, dangerous drug that is physically, mentally and emotionally destructive.

The Meth Strike Force is committed to educating the public about the many dangers of meth through their website: www.2stopmeth.org. This strike force is comprised of representatives from diverse fields, such as behavioral health, medicine, law enforcement, probation department, and the judicial system, among others.

Their website contains a vast amount of information about the health and safety hazards meth poses to the user and to the community.

The following highlights some of the destructive effects of meth as reported in the Task Force's website under the heading "What are the effects of Meth?"

Meth users can have serious health problems, including having symptoms similar to Parkinson's and Alzheimer's disease. Meth is a very powerful drug that stimulates the central nervous system, and users can suffer both short-term and long-term damage to their brains.

"Methamphetamine releases high levels of the neurotransmitter dopamine, which stimulates brain cells, enhancing mood and body movement. It also appears to have a neurotoxin effect, damaging brain cells that contain dopamine and serotonin, another neurotransmitter. Over time, methamphetamine appears to cause reduced levels of dopamine, which can result in symptoms like those of Parkinson's disease, a severe movement disorder. Research shows that high doses of meth damage neuron cell-endings. Dopamine- and serotonin-containing neurons do not die after methamphetamine use, but their nerve endings are cut back and re-growth appears to be limited," the website reports.

Effects of short-term meth use include increased heart rate, increased blood pressure, elevated temperature, wakefulness, nervousness, anxiety, and insomnia. Also, the drug causes increased attention, decreased appetite, decreased fatigue, increased activity, irritability and/or aggression, which can last eight to 24 hours. According to the website, the most dangerous stage of meth abuse is "when the drug use has produced psychosis ('tweaking')."

"A user who is tweaking has probably not slept in three to15 days, and consequently will be extremely irritable and paranoid. A tweaker does not need provocation to behave or react violently, but confrontation increases the chances of violent reaction. If the tweaker is using alcohol, his negative feelings and associated dangers intensify."

Chronic meth use can also cause "paranoia, hallucinations, repetitive behavior (such as compulsively cleaning, grooming or disassembling and assembling objects), and delusions of parasites or insects crawling under the skin. Users can obsessively scratch their skin to get rid of these imagined insects," the website said.

Further, chronic, high-dose meth abusers tend to be "undernourished with a gaunt appearance" and have "poor hygiene and rotten teeth and suffer from extreme paranoia." Meth users also experience "increased heart rate and blood pressure, which can result in irreversible damage to blood vessels in the brain and produce strokes."

"Long-term use, high dosages, or both can bring on full-blown toxic psychosis (often exhibited as violent, aggressive behavior). This violent, aggressive behavior is usually coupled with extreme paranoia. In the form of paranoia, hallucinations, mood disturbances, and repetitive motor activity), increased risk of convulsions, heart attacks, and weight loss. Meth can also cause cardiovascular collapse and death," the website said.

For women who are pregnant, "meth use can cause premature labor, detachment of the placenta, and low birth weight babies with possible neurological damage." Also, intravenous drug users can suffer from "AIDS, hepatitis, infections and sores at the injection site along with infection of the heart lining and valves."

Meth users under the influence often become agitated and feel wired. "They may be friendly and calm one moment, angry and terrified the next. Some feel compelled to repeat meaningless tasks, such as taking apart and reassembling bits of machinery. Others may pick at imaginary bugs on their skin. Hard-core methamphetamine addicts get very little sleep and they look like it," the site said.

The effects of meth also has a significant impact on children. "Butte County ranks third statewide in the number of children being detained from methamphetamine laboratories, with a total of eleven children rescued from meth lab sites. However, the Butte County Interagency Narcotics Task Force reports that in 2003, there was a total of 96 Drug Endangered Children investigations in which 223 children were rescued."

Statistics shared by the Task Force include numbers that show meth use is on the rise.

"Methamphetamine is no doubt the drug of choice here in Butte County. From January of 2003, through early September of 2004, 2,134 clients were seen by the Butte County Department of Behavioral Health Alcohol and Drug Services, for a primary diagnosis of Methamphetamine abuse and dependence.

"Of those 2,134 clients, 1,086 were unique and/or new to Drug and Alcohol Services. The remaining 1,048 were clients returning to services for further substance abuse treatment. The latter two figures show that not only is Meth addiction spreading through our county like a wind driven wildfire but, more importantly, it gives us a glimpse of how difficult it can be to remain abstinent/clean and sober once addicted to methamphetamine. For a majority of our clients it becomes a life long battle," the Task Force's website concluded.

Source: Paula M. Felipe. Educating the public about the dangers of meth. Mercury-Register Online(26 January 2006) [FullText]

"A compound in British black-currants can prevent Alzheimer’s disease. New research from New Zealand says black currants contain a powerful substance that protects the brain and researchers say this could eventually lead to a drug that helps guard against Alzheimer’s. Black-currants are hard to find in the United States but boysenberries have a similar compound."

Source: CBS3 Philadelphia (24 January 2006) [FullText]

Compounds in blackcurrants could prevent Alzheimer's disease and the characteristics of British berries suggest they do it best, writes Jennifer Rohn in Chemistry & Industry magazine.

New research led by Dilip Ghosh of the Horticulture and Food Research Institute in New Zealand, shows that compounds in blackcurrants have a potent protective effect in cultured neuronal cells against the types of stress caused by dopamine and amyloid-ß, a peptide associated with Alzheimer's disease.

'These compounds also work in hippocampal cells taken straight from the brain,' researcher James Joseph of Tufts University told Chemistry & Industry. James says that the effect will likely be reproduced in the human body and that blackcurrants could help prevent or significantly delay the onset of Alzheimer's.

Blackcurrants and boysenberries, more common in the US, both contain anthocyanins and polyphenolics. British blackcurrants are bred to be darker, which means they have more anthocyanins and are likely to be more potent.

Compounds from these berries are already known to act as antioxidants, but a role in neuroprotection has not been demonstrated previously, according to the researchers.

The mechanism of action is unclear. But James said: 'We have evidence that the compounds protect against Alzheimer's by influencing the early gene expression in learning and memory, which influences cell signaling pathways that help neuronal cells communicate with each other.'

Dilip's team recently demonstrated the potent protective effect of blackcurrant compounds on cultured human promyeloyte and neuroblastoma cells assaulted by hydrogen peroxide (JSFA doi: 10.1002/jsfa.0247).

http://www.soci.org

Source: Compounds in blackcurrants could prevent Alzheimer's disease. Medical Research News (23 Jan 2006) [FullText]

Drug discovery researchers at Northwestern University have developed a novel orally administered compound specifically targeted to suppress brain cell inflammation and neuron loss associated with Alzheimer's disease.

The compound is also rapidly absorbed by the brain and is non-toxic - important considerations for a central nervous system drug that might need to be taken for extended periods.

As described in the Jan. 11 issue of the Journal of Neuroscience, the compound, called MW01-5-188WH, selectively inhibits production of pro-inflammatory proteins called cytokines by glia, important cells of the central nervous system that normally help the body mount a response, but are overactivated in certain neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, stroke and traumatic brain injury.

The compound was designed and synthesized in the laboratory of D. Martin Watterson at Northwestern University Feinberg School of Medicine, using a synthetic chemistry platform developed in his lab by researchers at the Northwestern University Center for Drug Discovery and Chemical Biology (CDDCB) for the rapid discovery of new potential therapeutic compounds.

Watterson is co-director of the CDDCB, the J.G. Searle Professor of Molecular Biology and Biochemistry and professor of molecular pharmacology and biological chemistry at the Feinberg School.

The efficacy and safety of the compound in an animal model of Alzheimer's disease was evaluated in collaboration with Linda J. Van Eldik, co-director of the CDDCB and professor of cell and molecular biology at Feinberg.

Besides providing a lead compound for drug development, the study has important implications for drug discovery in neurodegenerative diseases in general because it provides proof of concept that targeting over-production of cytokines by activated glia is a viable approach that has the potential to modulate disease onset and progression, the researchers said.

Decline of cognitive functions linked to the part of the brain called the hippocampus is a clinical hallmark of Alzheimer's disease. The report demonstrates that targeting excessive glial activation can suppress brain inflammation and neuron dysfunction in the hippocampus and protect against cognitive decline in an animal model.

Neuron dysfunction can lead to further glia activation and contribute to further exacerbation of the disease process. The Northwestern researchers found that 188WH and related compounds slowed or reversed the progression of the neuroinflammatory cascade and reduced human amyloid beta-induced glia activation in a mouse specially designed to develop many of the signs of Alzheimer's disease, including neuroinflammation, neuronal and synaptic degeneration and behavioral deficits.

The compound also restored normal levels of markers of synaptic dysfunction in the hippocampus, the area of the brain that helps regulate memory and is gradually destroyed in neurodegenerative diseases such as Alzheimer's. Treatment with the compound also attenuated Alzheimer's-like behavioral deficits in the mice that are due to injury to the hippocampus.

While previous research by the authors and many other investigators in the field has linked plaques, tangles and neuronal injury to synaptic dysfunction and cognitive decline, the direct linkage of glia to these processes and their potential as a selective target for new therapies has not previously been implicated so directly.

There are three key aspects of the report, Watterson said.

"First, a novel compound for development into a new class of Alzheimer's disease therapeutics that target disease has been described. Second, an innovative approach was used for the rapid and cost-effective discovery of orally bioavailable, safe and efficacious compounds, and this approach can be extended to other disease areas," Watterson said.

"Third, the design, synthesis and in vivo analyses were carried out by a new generation of young scientists trained in our educational program to instruct the next generation of interdisciplinary scientists," Watterson said.

Northwestern University patented the compound designated 188WH and has exclusively licensed the patent rights to NeuroMedix, Inc., for clinical development.

http://www.northwestern.edu/

Source: Novel compound stops brain cell degeneration in Alzheimer's disease. Pharmaceutical News. (22 January 2006) [FullText]

Older adults who exercised at least three times a week were much less likely to develop dementia than those who were less active, according to a new study. The study did not demonstrate directly that exercise reduces risk of dementia, but it joins a growing body of observational research pointing to an association between exercise and cognitive decline, say scientists at the National Institute on Aging (NIA), a component of the National Institutes of Health (NIH), U.S. Department of Health and Human Services, which funded the study.


The research, reported in the January 17, 2006, issue of the Annals of Internal Medicine, was conducted by Eric B. Larson, M.D., Ph.D., and colleagues at the Group Health Cooperative (GHC), the University of Washington, and the VA Puget Sound Health Care System in Seattle, WA. Larson and co-investigators followed 1,740 GHC members age 65 or older for an average of 6.2 years between 1994 and 2003. When the study began, the participants -- all of whom were tested and found to be cognitively normal -- reported the number of days per week they engaged in at least 15 minutes of physical activity, such as walking, hiking, bicycling, aerobics, or weight training. Their cognitive function was then assessed, and new cases of dementia were identified, every 2 years. By the end of the study, the rate of developing dementia was significantly lower for those who exercised more -- 13.0 per 1,000 "person years" for those who exercised three or more times weekly, compared with 19.7 per 1,000 "person years" for those who exercised fewer than three times per week -- a 32 percent reduction in risk.

"Physical activity has been shown to be beneficial for health and aging in a number of areas," says Dallas Anderson, Ph.D., program director for population studies in the Dementias of Aging Branch of NIA's Neuroscience and Neuropsychology of Aging Program. "This emerging association between exercise and cognitive health is increasingly important to understand." The NIA is beginning to support clinical trials which seek to test exercise for its direct effect on cognitive function. Such research, Anderson says, should help sort out whether exercise reduces risk of cognitive decline or whether other factors related to exercise, such as increased social interaction, play a role. Additional study also may provide information on the possible merits of varying types of exercise.

Source: Exercise Associated With Reduced Risk Of Dementia In Older People. Science Daily (19 January 2006) [FullText]

A new study in mice suggests that Alzheimer's disease (AD) may be triggered when adult neurons try to divide. The finding helps researchers understand what goes wrong in the disease and may lead to new ways of treating it. The study was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and appears in the January 18, 2006 issue of The Journal of Neuroscience.*

For unknown reasons, nerve cells (neurons) affected by AD and many other neurodegenerative diseases often start to divide before they die. The new study shows that, in animal models of AD, this abnormal cell division starts long before amyloid plaques or other markers of the disease appear. Cell division occurs through a process called the cell cycle. "If you could stop cell cycling, you might be able to stop neurons from dying prematurely. This could be a fresh approach to therapy for Alzheimer's and other diseases, including stroke, amyotrophic lateral sclerosis [also known as Lou Gehrig's disease], and HIV dementia," says Karl Herrup, Ph.D., of Case Western Reserve University in Cleveland, who led the study.

The researchers compared the brains of three different mouse models of AD to brains from normal mice, looking specifically for markers of cell cycling. They found that, in the AD mouse models, cell cycle-related proteins appeared in neurons 6 months before the first amyloid plaques or disease-related immune reactions developed in the brain. Many of the neurons also had increased numbers of chromosomes, which is typical of cells that have begun to divide. These changes were not seen in normal mice. The regions of the brain most affected by the neuronal cell cycling were the cortex and the hippocampus – the same regions most affected in AD. The cortex is important for thought and reasoning, while the hippocampus plays a key role in learning and memory. Some parts of the brainstem also showed evidence of cell cycling.

While the cell cycling appeared to be necessary for neurons to die, it was not an immediate cause of cell death in the mouse models of AD. Instead, the affected neurons appeared to live for many months in a near-functional state, with the mice showing only mild behavioral changes during that time. This suggests that another type of cellular problem, still unidentified, must damage the neurons in order for them to die.

The findings shed new light on the theory that the accumulation of amyloid beta in the brain causes the neuron death in AD. Because the abnormal cell cycling begins months before the formation of amyloid plaques, it is unlikely that the plaques themselves trigger the disease process. However, tiny clumps made up of several amyloid beta molecules (called micro-molecular aggregates) form before the plaques and may trigger the disease. Since the three mouse models tested in this study all had mutations in the gene that codes for amyloid precursor protein, the similarity between affected brain regions in these mice and in people with AD also supports the amyloid hypothesis.

While previous studies have linked AD to abnormal cell cycling, this is the first study to examine the link using standard mouse models of AD. The results indicate that the mice, which do not develop neurofibrillary tangles or the severe behavioral symptoms of AD, are accurate models of the early cellular processes that lead to the disease. "The cell cycle markers mimic the human situation rather well," says Dr. Herrup. "This opens a range of new experimental possibilities using the cell cycle events as indicators of neuronal distress."

Dr. Herrup and his colleagues are now trying to determine if feeding the mouse models the drug ibuprofen can stop abnormal cell cycling in neurons and halt neurodegeneration. Ibuprofen is an anti-inflammatory drug that reduces production of amyloid beta, and some studies have suggested that it may reduce the risk of AD. The researchers are also planning additional studies to identify why neurons start to divide when they are diseased and why entering the cell cycle appears to trigger cell death.


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The NINDS is a component of the National Institutes of Health (NIH) within the Department of Health and Human Services and is the nation's primary supporter of biomedical research on the brain and nervous system. The NIH is comprised of 27 Institutes and Centers. It is the primary Federal agency for conducting and supporting basic, clinical, and translational medical research, and investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

The work was conducted at Case Western Reserve University's Alzheimer's Disease Center, which is directed by Dr. Herrup and supported by the National Institute on Aging, also part of the NIH.

*YangY, Varvel NH, Lamb BT, Herrup K. Ectopic cell cycle events link human Alzheimer's disease and APP transgenic mouse models. The Journal of Neuroscience, January 18, 2005, Vol. 26, No. 3, pp. 775-784.

Source: Study links Alzheimer's disease to abnormal cell division. Eurekalert (17 Jan 2006) [FullText]

Regular exercise reduces the risk of memory disorders such as dementia and Alzheimer's disease, say scientists. Workouts may also help to delay progression of the condition in people who begin to develop these symptoms.

Researchers led by Eric Larson at the University of Washington studied the effect of exercise on the people suffering from such disorders and reportedly found it reduces risk by 40 per cent.

The study followed 1,740 people aged 65 and older over a six-year period. At the start of the study none showed signs of dementia. After six years, 158 participants had developed dementia, of which 107 had been diagnosed with Alzheimer's disease.

People who exercised three or more times a week had a 30 per cent to 40 per cent lower risk of developing dementia compared with those who exercised fewer than three times per week, it found.

Larson believes exercise may improve brain function by boosting blood flow to areas of the brain used for memory. The frailer a person, the more likely that exercise would help.

A regular gentle workout was enough to produce a positive effect - even for people aged over 65. Even if you're 75 and have never exercised before, you can still benefit by starting to exercise now, the study said.

Larson said walking for 15 minutes three times a week was enough to cut the risk.

Source: IANS. Workouts reduce risk of Alzheimer's disease. DNA Evolutions (17 January 2006) [FullText]

The genetic underpinnings of Alzheimer's may just have gotten a little clearer.

An international research team led by investigators at Washington University School of Medicine in St. Louis say they've identified a region of DNA lying on chromosome 10 that's strongly associated with Alzheimer's disease.

The finding narrows the search for a gene in that area that causes Alzheimer's. The study appears in the January issue of the American Journal of Human Genetics.

"There are a few genes that have been implicated in the development of early-onset Alzheimer's disease, but other than APOE, no genes have been found that increase risk for the more common, late-onset form of the disease," principal investigator Alison M. Goate, a professor of genetics in psychiatry at Washington University, said in a prepared statement.

"The region of DNA identified in our study showed evidence of replication in four independent series of experiments. I haven't seen a putative risk factor show such consistent results since the e4 variant of the APOE gene was identified as a risk factor for late-onset Alzheimer's disease more than 10 years ago," Goate said.

The region of chromosome 10 pinpointed by Goate and her team contains six genes.

"We don't know which of those genes is most likely to harbor this particular risk factor for Alzheimer's disease, but we're getting closer. We're now trying to nail down which one of these six genes is the most likely to be involved," Goate said.

She expects that a total of five to 10 genes eventually will be identified as possible risk factors for late-onset Alzheimer's. It's possible that chromosome 10 contains more than one of those genes.

More information: The U.S. National Institute on Aging has more about Alzheimer's disease.

Source: Scientists Close in on Alzheimer's Genes. HealthDay News (17 Jan 2006) [FullText]

On the occasion of the 100th anniversary of the discovery of Alzheimer' disease, the Federation of Quebec Alzheimer Societies is launching a message of hope to people with the disease and to their families. Over the last twenty years, significant progress has led to improvements in their quality of life. Today they can take advantage of new treatments and a variety of intervention programs, and gain access to community-based resources adapted to their needs. Moreover, growth in the concentration of research in this area gives grounds to hope for major breakthroughs in the course of the next few years. Although much remains to be done to offer people with Alzheimer's disease and their families better living conditions, some paths are opening up to them.

Promising research

Research now under way allows us to hope for the development of a remedy, in a few years' time, that will control this disease or at least check its progress. Explains Dr. Serge Gauthier, Professor in the departments of Psychiatry, Neurology and Neurosurgery and Medicine at McGill University and Director of the Alzheimer Disease Research Unit of the McGill Centre for Studies in Aging, the drugs currently available can control certain symptoms: "Generally speaking, they help maintain functional independence. The effect on symptoms lasts an average of a year or two. After that we find a progressive loss of effectiveness. Fortunately, a new medication exists for treatment of moderate to severe Alzheimer's disease. It can be used during the third year, and for most patients still at home."

Exercises to slow development of the disease

Much research under way in the area of neuropsychology is exploring the possibilities of cognitive re-education among people who are at risk of developing the disease. That re-education is aimed at enabling them to temporarily regain their autonomy. Raymond Girard, a person with Alzheimer's disease we spoke to, told us: "I regularly do mental activity to keep my brain working. I have a little trouble talking, so I read aloud, in both French and English, and that helps me somewhat."

Dr. Sylvie Belleville, Professor in the Department of Psychology at the Universite de Montreal and associate director for clinical research at the Institut Universitaire de Geriatrie de Montreal, explains that several strategies can be taught to people liable to develop the disease: "For example, they can learn to memorize names by focusing on visual imagery, learn to use memory aids in an effective way, learn to connect information, to memorize things that they already know and finally learn to organize the information that they must retain. When used appropriately, these strategies can slow the impact of the disease on the functioning and well-being of the person and teach him or her to better control the situation."

Adapted intervention programs

Other researchers have focused on the situation of family members who take care of an ailing relative. Nearly 25 percent of Canadians have a family member living with Alzheimer's disease,(1) and families care for their relative at home for an average of eight to ten years.(2)

Dr. Francine Ducharme, holder of the Desjardins Chair in nursing care for the elderly and families at the research centre of the Institut Universitaire de Geriatrie de Montreal, stresses the importance of adequate support: "Access to a psycho-educational intervention program that offers care and support and adaptation strategies that respond to their needs has positive effects on the mental health and the quality of life of caregivers in the family. That support enables them to enjoy a more harmonious experience with their loved one suffering from Alzheimer's disease."

Innovative community-based resources

"It's unfortunate, but families often wait too long to ask for help from those around them or from support organizations," says Nathalie Ross, Executive Director of the Federation of Quebec Alzheimer Societies. She explains that the Alzheimer societies that are members of the Federation have over the years set up a number of programs and activities to support and help care for people with Alzheimer's disease and their families: "Those resources are aimed at responding to the needs of families. They're based on a philosophy of humanist intervention that emphasizes respect for the relationships between persons with the disease and those around them, and considering the family as a partner. Additionally, everything is done to promote the establishment of a relationship of trust with caregivers so that persons with the disease can feel accepted and useful." She adds that respect for the pace, the dignity and the reality of the person is primordial and that caregivers must learn to set aside their personal needs in order to understand and respond to those of the person with the disease. They must also accept the integration of their reality, even if it does not correspond to the usual standards.

About the Federation of Quebec Alzheimer Societies

The Federation of Quebec Alzheimer Societies brings together 21 regional Alzheimer societies in Quebec and is a member of the Alzheimer Society of Canada. It has taken as its mission the alleviation of the personal and social consequences of Alzheimer's disease, the support of persons with the disease and of their families, the defence of their rights, the dissemination of information about Alzheimer's disease, the sensitizing of public opinion, and support for research.

For additional information or to make a financial contribution to the Alzheimer societies, call 1-888-MEMOIRE or visit the following Internet site: www.alzheimerquebec.ca.

(1) The Aluminium Association Alzheimer Disease Survey, Public Opinion Strategies, 1997.
(2) Thompson C. & Thompson, G. (2003). Support for Carers of People with Alzheimer's Type Dementia. In Cochrane Library, 3, 1-24. Oxford Update Software.

Source: ccnmatthews.com (10 January 2006) [FullText]

"The first study of the effects of testosterone on mood, behavior and psychological health in men with mild Alzheimer disease finds significant improvements in quality of life, as assessed by caregivers.

Led by neuroscientists at the UCLA Alzheimer Disease Research Center and detailed in an early online release of the peer-reviewed journal Archives of Neurology, the double blind, placebo-controlled study used caregiver assessments to evaluate quality of life and used a battery of tests administrated by clinicians to evaluate cognitive skills.

Alzheimer patients treated with testosterone showed significant improvement on a quality-of-life instrument that encompasses memory, interpersonal relationships, physical health, energy, living situation and overall well-being compared with patients who received a placebo, or inactive, medication. However, researchers found no significant differences in memory or other cognitive skills as assessed by tests administered by clinicians.

"The results suggest that testosterone replacement therapy holds potential for improving quality of life of Alzheimer patients and merits further testing with a larger group of patients and with a longer treatment period," said Dr. Po H. Lu, lead author and assistant clinical professor of neurology at the research center and the David Geffen School of Medicine at UCLA.

An estimated 4 million Americans are affected by Alzheimer disease, which causes memory loss, behavior changes and difficulties with thinking.

The 24-week study included 16 male patients diagnosed with mild Alzheimer disease and 22 healthy male control subjects. Each group was randomly subdivided into two treatment arms. One group received daily testosterone treatment in the form of hydroalcoholic gel (75 mg) and other received a gel with no active medication.

The research team assessed cognitive function using the Alzheimer Disease Assessment Scale -- Cognitive Subscale, California Verbal Learning Test, Block Design Subtest, Judgment of Line Orientation and Development Test of Visual-Motor Integration; neuropsychiatric symptoms using the Neuropsychiatric Inventory; global functioning using Clinician's Interview-based Impression of Change; and quality of life using the Quality of Life -- Alzheimer Disease Scale.

Among patients with the disease, the testosterone-treated group had significantly greater improvements in the scores on the caregiver version of the quality-of-life scale than those who received placebo. No statistically significant differences were seen in cognitive or other scores at the end of the study, though numerically greater improvement or less decline in measures of visual-spatial abilities were found in the group treated with testosterone.

In the healthy control group, a non-significant trend toward greater improvement in self-rated quality of life was observed in the testosterone-treated group compared with placebo treatment.

Primary funding was provided by the John Douglas French Alzheimer's Foundation. Additional funding was provided by the National Institute on Aging; the UCLA Alzheimer Disease Research Center; the Los Angeles-based Sidell-Kagan Foundation; the University of California, Irvine, Alzheimer's Disease Research Center; and the Memory and Aging Center at the University of California, San Francisco.

Testosterone and placebo gel were supplied by Marietta, Ga.-based Unimed Pharmaceuticals Inc.

In addition to Lu, other researchers involved in the study were Dr. Donna A. Masterman, Dr. Verna Porter, Dr. Jeffrey L. Cummings and Erin Rebak of UCLA; Ruth Mulnard and Carl Cotman of the University of California, Irvine; Dr. Bruce Miller and Dr. Kristine Yaffe of the University of California, San Francisco; and Dr. Ronald Swerdloff of Harbor-UCLA Medical Center.



###
The UCLA Department of Neurology encompasses more than a dozen research, clinical and teaching programs. These programs cover brain mapping and neuroimaging, movement disorders, Alzheimer disease, multiple sclerosis, neurogenetics, nerve and muscle disorders, epilepsy, neuro-oncology, neurotology, neuropsychology, headaches and migraines, neurorehabilitation, and neurovascular disorders. The department ranks No. 2 among its peers nationwide in National Institutes of Health funding.

The Alzheimer Disease Research Center (ADRC) at UCLA, directed by Dr. Jeffrey L. Cummings, was established in 1991 by a grant from the National Institute on Aging. Together with grants from the Alzheimer Disease Research Center of California grant and the Sidell Kagan Foundation, the center provides a mechanism for integrating, coordinating and supporting new and ongoing research by established investigators in Alzheimer disease and aging. The Memory Disorders and Alzheimer's Disease Clinic of the ADRC is an evaluation clinic for individuals over the age of 45 who are experiencing mild but gradually progressing cognitive or memory declines that are not related to other brain diseases such as strokes, tumors, infection, metabolic abnormalities, psychiatric disease or trauma."

Additional online resources:

David Geffen School of Medicine at UCLA: www.medsch.ucla.edu/
UCLA Department of Neurology: http:/neurology.medsch.ucla.edu/
Alzheimer Disease Research Center at UCLA: www.adc.ucla.edu/

Source: Science Daily News Release (10 January 2006) [FullText]

"Dr. Ira B. Black, a neuroscientist and brain researcher who became an early advocate for stem cell research and a founder of the Stem Cell Institute of New Jersey, died on Tuesday at a hospital in Philadelphia. He was 64.

The cause was an infection related to a tumor, his family said.

Dr. Black argued forcefully that medicine would gain from laboratory research involving stem cells taken from tissue and human embryos. He said the cells derived from embryos, while controversial, could constitute "the gold standard" in repairing damaged nerve cells and developing therapies to treat Alzheimer's disease, cancer and other ailments.

When, in 2004, New Jersey became the second state, after California, to adopt legislation approving stem cell research, Dr. Black was appointed the first director of the state-financed Stem Cell Institute of New Jersey. He was also chairman of the department of neuroscience and cell biology at the University of Medicine and Dentistry of New Jersey.

Dr. Black's own research involved investigations of neurons and brain function as well as the origins of neurons, the nerve cells found throughout the body. In 2000, Dr. Black and others reported that they had succeeded in forming cells similar to neurons from stem cells taken from the bone marrow of humans and rats. The experiment did not use cells derived from embryos, whose destruction in other types of stem cell research has angered abortion opponents.

The scientists added an antioxidant and watched the cells change into cells with the appearance and properties of neurons. Dr. Black recalled the discovery: "Over the course literally of minutes, the cells converted from rather pedestrian, flat, undistinguished stem cells into typical neuron-looking cells."

"We were disbelieving," he added.

Perry B. Molinoff, vice provost for research at the University of Pennsylvania, said that Dr. Black's results, published in The Journal of Neuroscience Research, were "an incredible achievement," in part because they hinted at the mechanism that allows stem cells to differentiate into cells intended for the brain, blood, liver and other organs.

Dr. Molinoff continued, "It was a finding of enormous importance because it spoke to a core question of Ira Black's work, which is uncovering the potential to treat diseases for which there are at present no therapies."

Dr. Black and others later transplanted the newly formed cells into the spinal cords and brains of laboratory rats and found that both the cells and the rats survived without ill effects.

The finding underscored his argument that stem cells could possibly act as a vehicle to introduce gene therapy or be employed to rally the body's existing stem cells.

As an administrator, Dr. Black expressed impatience with the scarcity of public financing for stem cell research and the seeming cross-purposes of federal and state legislation intended to control or encourage it. This month, New Jersey legislators decided to postpone proposals that would have provided about $600 million in state sponsorship for stem cell research.

"We hope we'll get patients out of bed and out of wheelchairs," he said in an interview in July, "and that's one of the reasons it's particularly frustrating to have a federal stance that inhibits this progress."

Ira Barrie Black was born in the Bronx. He attended the Bronx High School of Science and earned an undergraduate degree from Columbia. In 1965, he received his medical degree from Harvard.

From 1975 to 1990, Dr. Black was director of the division of developmental neurology at Cornell. He was the author of "The Changing Brain: Alzheimer's Disease and Advances in Neuroscience" (2002) and "Information in the Brain: A Molecular Perspective" (1991).

He was president of the Society for Neuroscience in 1992.

Dr. Black's marriage to Janet Linquist Black ended in divorce in 1999. He lived in Skillman, N.J., and Andes, N.Y.

He is also survived by a son, Reed, and by his fiancée, Janet Davis, both of Skillman."

Source: Jeremy Pearce. Dr. Ira B. Black, 64, Leader in New Jersey Stem Cell Effort, Dies. New York Times: NY Region (12 January 2006) [FullText]

University of Pittsburgh and University of California, Los Angeles imaging study establishes two forms of mild cognitive impairment

Mild cognitive impairment (MCI), a transitional stage between normal cognition and Alzheimer's disease, exists in two different forms, according to a study published today by researchers from the University of Pittsburgh School of Medicine and the University of California, Los Angeles in the Archives of Neurology.

Using a new imaging procedure that creates 3-D maps of the brain, researchers determined specific areas that had degenerated in people with MCI. Depending on the person's symptoms, more tissue was lost in the hippocampus, a brain area critical for memory and one of the earliest to change in Alzheimer's disease, indicating two different paths of progression to Alzheimer's disease. The finding could lead to better diagnosis and treatment of patients with MCI, perhaps delaying or preventing the onset of dementia.

MCI is categorized into two sub-types – currently distinguished based solely on symptoms. Those with MCI, amnesic subtype (MCI-A) have memory impairments only, while those with MCI, multiple cognitive domain subtype (MCI-MCD) have other types of mild impairments, such as in judgment or language, but also have either mild or no memory loss. Both sub-types progress to Alzheimer's disease at the same rate. Until now it was not known if the pathologies of the two types of MCI were different, or if MCI-MCD was just a more advanced form of MCI-A.

Researchers found that the hippocampus of the patients with MCI-A was 14 percent smaller than that of the healthy subjects, nearly as great as the 23 percent shrinkage seen in Alzheimer's disease. But, the hippocampus of those with MCI-MCD most resembled that of the controls, showing only 5 percent shrinkage.

Using highly accurate Magnetic Resonance Imaging (MRI) data from six patients with MCI-A, 20 with MCI-MCD and 20 with Alzheimer's disease who were seen at the University of Pittsburgh's Alzheimer Disease Research Center and 20 healthy controls, researchers created 3-D mesh reconstructions of each participant's hippocampus that allowed them to see where the hippocampus had deteriorated. This study is the first to use such modeling technology to visualize changes in the brains of people with MCI. Prior studies have only been able to measure the volume of the hippocampus and estimate atrophy through noticeable volume loss.

"These vibrant images produced by 3-D modeling have proven what we suspected – there are at least two transitional states that lead to Alzheimer's disease," said James T. Becker, Ph.D., a neuropsychologist and professor of psychiatry, neurology and psychology, at the University of Pittsburgh School of Medicine and lead author of the study. "Now we can investigate these pathways and develop treatments that, we hope, may slow or stop the progression of Alzheimer's."

Alzheimer's disease affects as many as 10 percent of people older than 65, and delaying or preventing the onset of dementia is an important medical priority. "We can now see the pattern of brain damage in people with MCI and we can use these new types of images to monitor how different therapies may be working," said Paul M. Thompson, Ph.D., associate professor of neurology, at the University of California, Los Angeles. "By imaging the brain like this, we can explore the progression of diseases, and see if therapies are protecting the brain."

This research was conducted by the Imaging Methods and Analysis in Geriatrics Research Group. Co-authors of this study from the University of Pittsburgh were: Simon W. Davis, department of psychiatry; Carolyn Cidis Meltzer, M.D., departments of radiology and psychiatry and Oscar L. Lopez, M.D., department of neurology. Contributing from UCLA were Kiralee M. Hayashi and Arthur W. Toga, Ph.D., both of the department of neurology.

The study was funded by grants from the National Institute on Aging, National Library of Medicine, National Center for Research Resources and National Institute of General Medical Sciences.

Source: EurekAlert (9 January 2005) [FullText]

"New drugs that are based on a compound found in the body may give renewed hope to stroke victims and sufferers of degenerative brain diseases such as Alzheimer’s as researchers are hopeful of a new therapeutic approach.

Current Alzheimers drugs are restricted in its effectiveness because of side effects. This new finding has generated a lot of excitement as it specifically targets the nerve cells avoiding other cell types. "Of even more importance, these drugs may be much less toxic than prior drugs in this class," said Professor Stuart Lipton, study author and director of the Centre for Neurosciences and Aging at the Burnham Institute.

This study represents the first reported evidence that this protective response can be activated directly in nerve cells to release antioxidants and counter oxidative stress, boding well for future research.

The US-Japanese research team, consisting of scientists from the Burnham Institute of Medical Research in La Jolla, California, and four Japanese universities, Iwate, Osaka City, Iwate Medical and Gifu Universities, experimented on the nerve cells in the brains of mice.

This approach works by inducing nerve cells in the brain and the spine to release natural antioxidants that protect nerve cells from stress and free radicals that lead to neurodegenerative diseases.

Until this discovery, researchers were unable to induce release of these specific antioxidants directly in nerve cells, at the site where damage and degeneration occurs.

In stroke and various neurodegenerative disorders, such as Alzheimer's disease and Lou Gehrig's disease, glutamate, an amino acid found in high quantities in the brain, is thought to accumulate.

At normal concentrations, glutamate acts as a neurotransmitter that nerves use to communicate. However, at excessive levels glutamate is toxic, resulting in over stimulation of nerve cells, known as excitotoxicity, and causing excessive stress on the nerve cells eventually ending in cell death.

However Lipton was quick to point out that the study had only been done in mice, and that a break through was a long way off.

Currently, 24.3 million people are currently estimated to have dementia, with 4.6 million new cases being diagnosed each year as the population ages. By 2040 the number is predicted to have risen to 81.1 million.

A report for Alzheimer's Disease International, published in The Lancet, said that the number of cases of dementia world-wide is likely to double every 20 years.

The report said most people living with dementia are in the developing world, with five million in China alone.

This compares with 4.8 million in Western Europe and 3.4 million in North America.

The paper detailing the findings of this study is entitled "Activation of the Keap1/Nrf2 Pathway for Neuroprotection by Electrophilic Phase II Inducers," is published in the January 17th issue of the Proceedings of the National Academy of Sciences."

Source: Wai Lang Chu. Drug induces nerves to repair themselves. In-PharmaTechnologist.com (10 January 2005) [FullText]

Barry Reisberg, MD, Professor of Psychiatry at New York University School of Medicine and Director of the Fisher Alzheimer's Education and Resources Program is the principal author of a one year study on the drug, memantine. The medication which has yielded success in treating patients with moderate to advanced cases of Alzheimer's disease over a 6 month period, now appears to be effective over a time span of one year. This study was funded by Merz Pharmaceuticals GmbH, Frankfurt, Germany.

Findings on memantine which were published in March 2003 in the New England Journal of Medicine, in moderate to severe Alzheimer's disease patients indicated the efficacy of memantine treatment over a 28 week double-blind trial period. This study was used as a pivotal trial in memantine's approval first in the E.U. in 2002, and subsequently in the U.S. in 2003 and, subsequently, went on the US market as Namenda. It is now used worldwide as the only approved treatment for the more advanced stages of Alzheimer's disease.

This study which appears in the January issue of the Archives of Neurology, examined the effects of continuing the memantine treatment for an additional 24 weeks of open label treatment in both the NEJM study patients and the placebo treated patients.

The findings indicate the continuing benefits over a one year period in the subjects who were originally receiving memantine treatment. Significant benefits in global, functional and cognitive outcomes examined were also found in the original placebo group. The results also indicate the continued, favorable tolerability of the memantine treatment over this extended period.

Dr. Reisberg believes that these results, obtained in patients with moderate to severe Alzheimer's disease, significantly extend the timeline of the previous findings.

ABOUT DR. BARRY REISBERG

Dr. Reisberg has served as the Director of the Fisher Alzheimer's Educational and Resources Program since its inception over 10 years ago. He is also the Clinical Director of the Silberstein Aging and Dementia Research Center at New York University School of Medicine, as well as an Adjunct Professor at the McGill University Faculty of Medicine in Montreal, Canada.

Dr. Reisberg was the first to describe many of the most important symptoms of Alzheimer's and the characteristic clinical course of the disease, with the Global Deterioration Scale (1982) and the Functional Assessment Staging measure (1984). His staging tools are presently governmentally mandated measures for certain purposes throughout the U.S., and elsewhere in the world.

Dr. Reisberg has been the recipient of numerous grants and awards for his pioneering research including a Lifetime Achievement Award for Research in Alzheimer's disease from the major worldwide organizations in 2004.

Since 1995, the Fisher Center for Alzheimer's Research Foundation's global research team has been dedicated to spearheading research into the cause, care, and cure for Alzheimer's disease. The Foundation now funds over 85 scientists worldwide under the direction of Nobel laureate Dr. Paul Greengard, headquartered at the Fisher Center for Alzheimemer's Disease Research at The Rockefeller University. It is a registered 501(c)(3) nonprofit organization with over 94% of every dollar raised directly supporting this research.

The Foundation earned the highest rating, 4 out of a possible 4 stars, from Charity Navigator, the leading independent evaluator of charities. Visit http://www.alzinfo.org for more information.

Source: PRNewswire (10 Janury 2006) [FullText]

The Seafood Industry Teams up With Meals on Wheels Association of America to Encourage its Nationwide Network to Meet the Recommended Weekly Servings of Seafood.

"The National Fisheries Institute (NFI) and Meals On Wheels Association of America (MOWAA) today launched a joint effort to promote the health benefits associated with including fish in a healthy, balanced diet.

The "Go Fish!" program theme is modeled after the popular card game and will provide thousands of MOWAA members, volunteers, clients, donors and staff a different "playing card" each week that will include recipe and meal preparation ideas, health and nutrition information and facts about fish. The first card, the King of Hearts, is available upon request.

"We know that many health benefits are derived when seafood consumption is increased and are pleased with the opportunity to share this information with our members because of our partnership with NFI," said Enid Borden, CEO of MOWAA. "It is our desire to promote better nutrition for seniors we serve and encourage them through our programs to put more fish in their diets."

NFI President John Connelly said, "Though seafood consumption is on the rise, Americans still only eat less than half the recommended servings of fish per week. Our partnership with Meals on Wheels will help the seafood community reach a broad group of Americans who need accurate information about why fish is healthy as well as techniques to handle and prepare these meals."

As detailed in the 2005 Dietary Guidelines for Americans and new food guide pyramid, the federal government recommends at least two servings of fish or seafood per week. The guidelines specifically mention the tremendous health benefits of fish and shellfish -- such as omega-3 fatty acids -- that can "reduce the risk of mortality from cardiovascular disease."

Studies also show that fish is "brain food." Research published in the Archives of Neurology conducted by the Rush Institute for Healthy Aging found dietary intake of omega-3 essential fatty acids and weekly consumption of fish may reduce the risk of Alzheimer's disease. Numerous studies show that omega- 3s also protect against coronary heart disease and stroke and aid in the neurological development of unborn babies.

NFI is the leading trade association for the fish and seafood industry whose members represent a variety of businesses ranging from the water to the table. For more information visit our website at http://www.AboutSeafood.com.

Meals On Wheels Association of America (MOWAA) is the oldest and largest organization in the United States representing those who provide meal services to people in need. MOWAA works toward the social, physical, nutritional, and economic betterment of vulnerable Americans so that "no senior goes hungry."® For more information visit http://www.mowaa.org."

Source: New 'Go Fish!' Program Brings Health Benefits of Fish to Americans' Doorsteps. PRNewsWire : biz.yahoo.com (4 January 2005) [FullText]

Alzheimer's is a progressive disease that has no cure yet. As research continues, doctors and patients are both hoping for a breakthrough. Now, doctors are getting close to one with an unlikely treatment.

Harvey and Kay Ottinger have shared 50 years of homemade meals, so you can bet Kay noticed when Harvey's memory started slipping. She signed them both up for a memory test.

"We both went down there, and they screened us. Kay passed it very well, but I didn't pass," Harvey says. He enrolled in a study to test the effects of nicotine on memory loss.

Paul Newhouse, M.D., Professor of Psychiatry at University of Vermont in Burlington, says, "Nicotine can improve learning. It can improve attentional performance."

For the study, patients with mild memory loss will wear a nicotine patch or placebo patch for a year. The hope is that nicotine can replace the chemicals lost as memory fades.

Dr. Newhouse says researchers think it would provide a way to treat the earliest signs of memory loss and attentional loss. The patch does not cause addiction. In fact, nicotine is also being studied to treat schizophrenia, ADHD and Parkinson's.

Dr. Newhouse is excited about nicotine's potential for Alzheimer's. "This is the kind of work that makes my career and life and work seem meaningful," he says.

Harvey's not sure if he's on the real thing or a placebo, but either way, he says being in the study has already helped. "I take extra precautions like writing down certain things that I have to do," he says. "I feel good, yeah." And if he does forget something, Kay is right by his side to remind him.

Dr. Newhouse says nicotine does not pose any safety concerns and is only addictive when it's combined with tobacco. Nicotine patches may not be a practical treatment for long-term use, so drugs are being developed that mimic what it does in the brain.

The University of Vermont is one out of three centers studying nicotine. The other two centers are Duke University and Georgetown University.

Source: Ivanhoe Newswire. Nicotine for Memory Loss. (5 January 2006) [FullText]

"Chemists in Chile and Spain have identified a new approach for the possible treatment of Alzheimer's disease that they say has the potential to destroy beta-amyloid fibrils and plaque -- hypothesized to contribute to the mental decline of Alzheimer's patients. The researchers say the new technique, which they call a type of "molecular surgery," could halt or slow the disease's progress without harming healthy brain cells. The research is scheduled for publication in the Jan. 11 issue of the American Chemical Society's Nano Letters.

Using test tube studies, the scientists attached gold nanoparticles to a group of beta amyloid fibrils, incubated the resulting mixture for several days and then exposed it to weak microwave fields for several hours. The energy levels of the fields were six times smaller than that of conventional cell phones and unlikely to harm healthy cells, the researchers say. The fibrils subsequently dissolved and remained dissolved for at least one week after being irradiated, indicating that the treatment was not only effective at breaking up the fibrils but also resulted in a lower tendency of the proteins to re-aggregate, according to the researchers.

The same approach also holds promise for treating other neurodegenerative diseases that involve protein aggregation, including Parkinson's and Huntington's, says study leader Marcelo J. Kogan, of the University of Chile in Santiago. He says that the approach is similar to that of another experimental technique that uses metallic nanoparticles to label and destroy cancer cells. Animal studies are planned, Kogan says.

There's currently no cure for Alzheimer's disease and no one is sure of its exact causes. The disease affects an estimated 4.5 million people in the United States, according to the National Institute on Aging. That figure is expected to rise dramatically as the population ages, experts predict.

The American Chemical Society — the world's largest scientific society — is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio."

The online version of the research paper cited above was initially published Dec. 17 on the journal's Web site. Journalists can arrange access to this site by sending an e-mail to newsroom@acs.org or calling the contact person for this release."

Source: EurekAlert.com (4 January 2006) [FullText]

"Sunnybrook & Women's, together with British and Canadian researchers, have led a study that suggests a new drug has the potential to safely modify and slow down the progression of Alzheimer's disease (AD) in its early stages.

Flurizan is an investigational drug being studied in patients with mild-to-moderate stages of the disease. "This is one of the first drugs to show the potential to not just treat the symptoms of AD, but also to slow down the disease itself if it is in the mild stage," says Dr. Sandra Black, co-principal investigator of the study, head of Neurology at Sunnybrook and Women's College Health Sciences Centre and internationally renowned researcher in AD. "As a phase 2 clinical trial, these results are preliminary, but they give some hope for the development of a new treatment for AD."

The study results were presented recently by Dr. Black at Neuroscience 2005, the Society for Neurosciences' 35th annual meeting in Washington. The findings indicate a significant trend of lesser decline in activities of daily living and global function, which includes memory, judgment, and hobbies.

Over a one-year period in both Canada and the U.K., Flurizan was tested in 207 patients with mild-to-moderate severity of Alzheimer's disease, which means they were in the earlier stages of the disease as defined by the Mini-Mental State exam; a score of 15 to 26 out of possible 30. A patient with mild AD is fairly independent but experiences some difficulty with more demanding activities such as handling finances. Patients who decline to moderate AD require more prompting for some basic self-care activities, such as bathing and brushing teeth.

The patients were randomized into three groups: two received treatment (either 400 or 800 mg), and one received placebo. All three groups were tested using communication and memory tests such as naming pictures, remembering a list of items and performing tasks such as addressing and stamping a letter.

The study results found the optimum dose is the higher dose of 800 mg, and the target population is people in the mild stages rated as 20 to 26 (not so much the moderate stages). The drug appears to be well tolerated with no serious drug-related side effects. The authors also note that the one-year study was important for detecting significant changes, as most studies in AD have only been for a six-month period. "We found it is best to give the drug in the earlier stages of the disease," says Dr. Black. "The effects only began to show around the nine-month point as it is a slow process."

Amyloid is a sticky toxic protein that gradually deposits between nerve cells in the brain in Alzheimer's disease, damaging and killing cells. "It is important to stop this abnormal buildup," says Dr. Black. Flurizan has an anti-amyloid action, gradually reducing the buildup of the production of the toxic protein, and potentially slowing progression of the disease.

At the completion of the phase 2 study, over 80 per cent of eligible patients enrolled in a one-year partly-blinded continuation treatment study at the Canadian sites to retrieve more information on the drug's safety and to further identify the best dosage. The study is currently in its last few months, with patients participating in the treatment trial for a total of 24 months.

Based on the trial's preliminary results, a larger phase 3 clinical trial is now currently underway in the U.S., with hopes for a second Canadian and European trial in the late spring of 2006. "If proven in the phase 3 study, it might bring real hope to modify disease course. Hopefully, it could be taken safely for many years," says Dr. Sandra Black. With further research, it may prove to be useful as a regular preventative medication that high-risk patients would take to delay the onset of AD, similar to medications that help to prevent heart disease or stroke in high-risk patients.

Dr. Gordon Wilcock, a geriatrician in the U.K., is the co-principal investigator of the study. The trial was peer reviewed by the Consortium of Canadian Centres for Clinical Cognitive Research (C5R). Flurizan is produced by Myriad Pharmaceuticals, an American bio-technology company. Myriad chose 31 research institutions in Canada and the U.K. to lead the Phase 2 developmental trial, with the majority of sites in Canada.

About Alzheimer's Disease

Alzheimer's disease is a progressive neurological disease of the brain that leads to the irreversible loss of brain cells and tissue. AD causes progressive impairment in memory, judgment, decision-making, orientation to physical surroundings, and language. Alzheimer's disease is the most common of all neurodegenerative diseases; over 360,000 Canadians (1 in 20) over 65 have Alzheimer's and related dementias. This number is expected to double in the next 20 years, as the population ages. There is currently no cure.

About Sunnybrook and Women's College Health Sciences Centre
Sunnybrook and Women's College Health Sciences Centre is transforming health care through the dedication of its more than 10,000 staff members, physicians and volunteers. Sunnybrook & Women's proudly provides care for hundreds of thousands of patients each year, including Canada's war veterans, through world-class programs in cancer, cardiac, musculoskeletal, neurosciences, perinatal and gynaecology, trauma and critical care, and aging and population health. The hospital has a special emphasis on improving women's health and patient safety throughout all of its programs and services. A full affiliation with the University of Toronto and proven track-record of conducting leading-edge research and teaching the latest advances in healthcare, distinguishes Sunnybrook & Women's as one of Canada's premier academic health sciences centres."

For further information: www.sw.ca/

Source: New Drug Looks Promising to Fight Early Alzheimer's. CCNMatthews (4 January 2006) [FullText]

"A new UCLA imaging study shows that age-related breakdown of myelin, the fatty insulation coating the brain's internal wiring, correlates strongly with the presence of a key genetic risk factor for Alzheimer disease.

The findings are detailed in the January edition of the peer-reviewed journal Archives of General Psychiatry and add to a growing body of evidence that myelin breakdown is a key contributor to the onset of Alzheimer disease later in life.

In addition, the study demonstrates how genetic testing coupled with non-invasive evaluation of myelin breakdown through magnetic resonance imaging (MRI) may prove useful in assessing treatments for preventing the disease.

"Myelination, a process uniquely built up in humans, arguably is the most important and most vulnerable process of brain development as we mature and age. These new findings offer, for the first time, compelling genetic evidence that myelin breakdown underlies both the advanced age and the principal genetic risks for Alzheimer disease," said Dr. George Bartzokis, professor of neurology at UCLA's David Geffen School of Medicine.

"The human brain functions as a high-speed Internet system," said Bartzokis, director of the UCLA Memory Disorders and Alzheimer Disease Clinic and Clinical Core director of the UCLA Alzheimer Disease Research Center. "The quality of the brain's connections is key to its speed, bandwidth, fidelity and overall on-line capability."

Myelin is a sheet of lipid, or fat, with very high cholesterol content -- the highest of any brain tissue. The high cholesterol content allows myelin to wrap tightly around axons, speeding messages through the brain by insulating these neural "wire" connections.

As the brain continues to develop in adulthood and as myelin is produced in greater and greater quantities, cholesterol levels in the brain increase and eventually promote the production of a toxic protein that attacks the brain. The protein attacks myelin, disrupts message transfer through the axons and eventually can lead to the brain/mind-destroying plaques and tangles visible years later in the cortex of Alzheimer patients.

The Apolipoprotein E (ApoE) genotype is the second most influential Alzheimer risk factor, after only advanced age. The study used MRI to assess myelin breakdown in 104 healthy individuals between ages 55 and 75 and determine whether the shift in the age at onset of Alzheimer disease caused by the ApoE genotype is associated with age-related myelin breakdown.

The results show that in later-myelinating regions of the brain, the severity and rate of myelin breakdown in healthy older individuals is associated with ApoE status. Thus both age, the most important risk factor for Alzheimer disease, and ApoE status, the second-most important risk factor, seem to act through the process of myelin breakdown."

Funding for the research was provided by grants from the National Institute of Mental Health, the National Institute on Aging, the California Department of Health Services, the Sidell Kagan Foundation and the Department of Veterans Affairs.

Other UCLA neuroscientists involved in the study included Po H. Lu, Dr. Daniel H. Geschwind, Nancy Edwards, Jim Mintz and Dr. Jeffrey L. Cummings.

The UCLA Department of Neurology encompasses more than a dozen research, clinical and teaching programs. These programs cover brain mapping and neuroimaging, movement disorders, Alzheimer disease, multiple sclerosis, neurogenetics, nerve and muscle disorders, epilepsy, neuro-oncology, neurotology, neuropsychology, headaches and migraines, neurorehabilitation, and neurovascular disorders. The department ranks No. 2 among its peers nationwide in National Institutes of Health funding.

The Alzheimer Disease Research Center at UCLA, directed by Dr. Jeffrey L. Cummings, was established in 1991 by a grant from the National Institute on Aging. Together with grants from the Alzheimer's Disease Research Center of California and the Sidell Kagan Foundation, the center provides a mechanism for integrating, coordinating and supporting new and ongoing research by established investigators in Alzheimer disease and aging. The Memory Disorders and Alzheimer's Disease Clinic of the Alzheimer Disease Research Center is an evaluation clinic for individuals over the age of 45 who are experiencing mild but gradually progressing cognitive or memory declines that are not related to other brain diseases such as strokes, tumors, infection, metabolic abnormalities, psychiatric disease or trauma.

Additional online resources:

David Geffen School of Medicine at UCLA: http://www.medsch.ucla.edu/.
UCLA Department of Neurology: http://neurology.medsch.ucla.edu/.
Alzheimer Disease Research Center at UCLA: http://www.adc.ucla.edu/.

Source: Imaging study links key genetic risk for Alzheimer's disease to myelin breakdown (2 January 2006) [FullText]