Alzheimer's Club

Alzheimer's Disease Set to Explod. Prediction: 106 Million Alzheimer's Patients by 2050

WebMD USA, by Daniel J. DeNoon (11 June 2007) -- Today, 26.6 million people worldwide suffer Alzheimer's disease. In just over 40 years, that number will quadruple to more than 106 million patients -- and 43% of them will need full-time care in nursing homes. This grim prediction of the global burden of Alzheimer's disease comes from Johns Hopkins researcher Ron Brookmeyer, PhD, and colleagues. The researchers base their forecast on a complex computer model fed United Nations population projections and data on Alzheimer's disease. "We face a looming global epidemic of Alzheimer's disease as the world's population ages," Brookmeyer says in a news release. "By 2050, one in 85 people worldwide will have Alzheimer's disease." The only good news from the computer model is that if new ways are found to slow the disease, it would significantly reduce the global burden of Alzheimer's -- even if these new treatments had only modest effects. Delaying Alzheimer's onset by just one year would reduce the 2050 case load by 12 million patients. But not all breakthroughs are equal. If researchers succeed in slowing Alzheimer's progression as well as delaying onset, there would be only 9.2 million fewer cases by 2050 -- because people with the disease would survive longer. "The worldwide costs will be huge," Brookmeyer and colleagues warn. Currently, nearly half of the people with Alzheimer's disease live in Asia. That proportion is expected to grow to 59% by 2050, with nearly 64 million cases. Brookmeyer's reported the grim numbers to the Second Alzheimer's Association International Conference on Prevention of Dementia, held June 9-12 in Washington. The findings also appear in the Alzheimer's Association journal Alzheimer's & Dementia.

Myriad Genetics Presents Mathematical Comparison of Disease Modification Trial Designs at Alzheimer's Conference. Current Flurizan Phase 3 Study Design May Demonstrate Disease Modification

Salt Lake City, UT, Market Wire (11 June 2007) -- Myriad Genetics announced today that it presented a mathematical comparison of a "Staggered Start" and a "Randomized Withdrawal" clinical trial design with a "Natural History Staggered Start" clinical trial design at the Alzheimer's Association Prevention Conference held June 9 - 12, 2007, in Washington, D.C. The analysis demonstrates that the "Natural History Staggered Start" trial design currently being used in the Flurizan Phase 3 study can provide the same level of disease modification support as the cross-over trial designs, which are challenged by ethical concerns, dropout bias and complications. A disease modifying therapy for Alzheimer's disease (AD) is one that has an impact on the underlying pathology of the disease and thus slows the rate of a patient's decline over the course of long-term treatment. In contrast, the currently available AD medicines are believed to treat the symptoms of AD without impacting the underlying disease process or providing long lasting benefit. The development of robust methods to demonstrate disease modification in AD clinical trials has been a controversial issue in the field, and to date, there have been no studies that provide convincing evidence of disease modification in AD. Two clinical trial designs that could provide evidence for disease modification were originally proposed for AD studies over 10 years ago by Paul Leber, then the head of the Division of Neuropharmacological Drug Products of the FDA. These designs have come to be known as the "Randomized Withdrawal" and "Staggered Start" designs and are based on measuring clinical outcomes in a cross-over type study. In the randomized withdrawal design, patients are withdrawn from therapy after a defined period to determine whether the long-lasting benefit to the patient is maintained, demonstrating disease modification, or if the patient drops back to the level of patients on placebo for the duration of the study. In a staggered start design, one group of patients receives the active study drug for the entire study period, while a second group initially receives placebo and then later is given the active drug. If the second group fails to "catch up" in the level of performance of the first group, this is taken to be evidence for a disease modifying effect of the drug. Unfortunately, these designs are difficult to implement and have rarely been used in clinical trials as they are complicated by very long study durations, leading to high dropout rates that introduce biased results, as well as presenting ethical concerns unacceptable to patients and their families. A team of biostatisticians and mathematicians at Myriad, led by Suzanne Hendrix, Ph.D., Sasha Gutin, Ph.D., and Scott Horton, has proposed an alternative strategy designated the "Natural History Staggered Start" analysis, that compares the slopes of decline of drug treated patients with those of patients receiving placebo and corrects for the severity of disease at baseline. The mathematical analysis presented at the Alzheimer's Association AD Prevention Conference demonstrates that this trial analysis methodology is mathematically equivalent to the "Staggered Start" and "Randomized Withdrawal" designs and provides the same level of evidence of a disease-modifying drug effect in a clinical trial that is not subject to the above-mentioned complications, bias and ethical challenges of the previous designs. "We are excited about this persuasive mathematical comparison of clinical trial designs," said Adrian Hobden, PhD, President of Myriad Pharmaceuticals, Inc. "We believe that this mathematical proof, coupled with the Flurizan trial design may strengthen the Company's position with the FDA in favor of a disease modification label for Flurizan..."

New test may help predict Alzheimer's disease

OCRegister - Orange County, CA, USA (11 June 2007 by Maggie Fox, Reuters, Washington, DC) -- New tests involving blood and brain scans can detect symptoms of Alzheimer's disease, and brief appraisals of real-life functioning can predict who is likely to develop it, researchers said on Sunday. The tests will be critical, experts told a meeting on Alzheimer's disease, because more than 26 million people now have the brain-wasting disease and this number will quadruple, to 106 million, by 2050. "By 2050, 1 in 85 persons worldwide will have Alzheimer's disease," said Ron Brookmeyer of Johns Hopkins University, who led the study on how many people have the disease. No drugs can significantly affect Alzheimer's disease, although four have a very modest impact if given early on. The disease is very difficult to detect until it has progressed from mild memory loss to clear impairment. Patients eventually lose all ability to care for themselves. Detecting the disease early can help patients and their families plan better for the future but can also help researchers develop drugs to treat and perhaps even prevent the disease. Anders Lonneborg and colleagues of DiaGenic, a biotech company based in Oslo, Norway, found a set of 96 genes that look different in the blood of Alzheimer's patients when compared to the same genes in healthy people. Their study of more than 100 older people, half from memory clinics and half from senior centers, found Alzheimer's accurately 85 percent of the time.
They identified genes related to the immune system, to inflammation and to cell division. The company has applied to regulators in the United States and Europe to approve the test, Lonneborg told a meeting of the Alzheimer's Association in Washington...

Biologic Agent from Elan/Wyeth Will Drive the Alzheimer's Disease Drug Market to More Than Triple by 2016, Reaching $8.8 Billion

Earthtimes.org: USA WALTHAM, Mass., (11 June 2007, by PRNewswire) -- Decision Resources, Inc., one of the world's leading research and advisory firms focusing on pharmaceutical and healthcare issues, finds that Elan/Wyeth's bapineuzumab, the first biologic agent for the treatment of Alzheimer's disease, will drive the Alzheimer's disease drug market to more than triple by 2016, reaching $8.8 billion. According to the new Pharmacor report Alzheimer's Disease, bapineuzumab -- a monoclonal antibody that is poised to begin Phase III trials and is expected to launch by 2011 in the United States and Europe -- will account for more than $5 billion in sales in 2016. A second monoclonal antibody, Eli Lilly's LY-2062430, may also launch by 2016 and contribute to market expansion. The report finds that bapineuzumab, Neurochem's Alzhemed, and Myriad Genetics' Flurizan -- three disease-modifying therapies that will launch over the next several years -- will account for 82% of Alzheimer's disease drug sales in 2016. Bapineuzumab will garner 61% of sales, while Alzhemed and Flurizan will garner 13% and 8%, respectively. However, the report finds that significant safety concerns may limit the overall sales potential of bapineuzumab. "The launch of bapineuzumab will be the most important factor driving growth in the Alzheimer's disease drug market," said Nitasha Manchanda, Ph.D., analyst at Decision Resources. "Despite being priced considerably lower than monoclonal antibodies in other markets, we expect bapineuzumab to enter the market priced nearly eightfold higher than current small molecule therapies. Nevertheless, we anticipate significant uptake of this agent -- particularly in patients with mild Alzheimer's disease -- despite the safety concerns. Alzhemed and Flurizan, both in Phase III development, have shown modest efficacy in trials to date and are likely to offer a better safety profile than bapineuzumab."

'Natural Protection' To Reduce Spread Of Alzheimer's Disease Possible

Science Daily (press release) - USAScience Daily -- Although numerous drugs have been developed over the years to alleviate the symptoms of Alzheimer's disease, there is still no real cure to halt this progressive, neurodegenerative disorder that causes premature death of nerve cells in the deep brain nuclei, leading to dementia and death. A graduate student in biological chemistry at the Hebrew University of Jerusalem has, however, developed an approach that holds out promise of providing natural brain protection against the spread of this disease. For his work, Erez Podoly, a joint student of Dean of Science Prof. Hermona Soreq and the head of the Wolfson Center for Applied Structural Biology, Prof. Oded Livnah, has been named one of the winners of this year's Kaye Innovation Awards, which were presented on June 6 during the 70th meeting of the Hebrew University Board of Governors. Alzheimer's Disease afflicts 12 million people worldwide, and this figure is expected to almost double over the next 25 years, due to prolonged life expectancy. Alzheimer disease patients develop neurotoxic precipitates ("plaques"), composed of the amyloid beta (Aβ) peptide, which spread as fibrils in the brain and destroy nerve cells. (A peptide is short chain of amino acids).
The several drugs that have been developed for Alzheimer's disease serve to enhance neuronal function, suppress inflammation, block or reduce the generation of oxidative stress in the brain, or minimize cognitive damage. Unfortunately, however, it is still unknown as to how to halt the spread of the neurotoxic plaques.
Podoly, 34, a native New Yorker, and his colleagues set out to design a blocker for the neurotoxic effects of the Aβ peptide, using the Butyrylcholinesterase (BChE) protein, which was cloned and engineered in their lab. BChE's brain concentration increases with age, a fact overlooked so far, but which for Podoly and his colleagues seemed highly relevant to the progress of Alzheimer's. The researchers set out in their laboratory to see if they could chemically improve and intensify BChE's effect on the brain fibrils. The researchers were indeed able to show in the lab that BChE purified from human blood and short synthetic peptides of BChE were able to reduce fibril formation. However, supply limitations and health risks limit the value of blood serum-derived human BChE. Fortunately, a breakthrough was achieved when PharmAthene Inc., an American company, was able to produce engineered human BChE that was introduced into the milk of transgenic goats. Recently, in collaboration between the Hebrew University, Yissum -- the technology transfer company of the university -- and PharmAthene, Podoly and his colleagues have succeeded in demonstrating by several independent methods that the goat-derived BChE efficiently interacts with and reduces amyloid fibrils formation. They anticipate that recombinant human BChE produced in the milk of transgenic goats and/or synthetic peptides derived from BChE can become novel prophylactic or therapeutic agents for slowing the progression of senile plaque formations in the brain of Alzheimer's patients. Further research, leading to clinical tests on humans, is planned for the future. Note: This story has been adapted from a news release issued by The Hebrew University of Jerusalem.

Unexplained Late-life Weight Loss May Be Early Predictor Of Alzheimer's

Science Daily, USA (11 June 2007) - Unexplained weight loss late in life, when coupled with other biomarkers, may help to identify those at risk of Alzheimer's disease...

New findings show unexplained weight loss that precedes dementia by more than 10 years is associated with the severity of Alzheimer changes in the brain. Using data from the Nun Study, a prospective study of the causes of dementia in Catholic sisters, University of South Florida researcher James Mortimer, PhD, reported today that the most likely cause of the unexplained weight loss is the severity of the Alzheimer changes in the brain rather than an eating disorder or other condition associated with declining cognition. Dr. Mortimer presented the findings at the Alzheimer's Association International Conference on the Prevention of Dementia in Washington, DC. Although a previous study showed that individuals with lower weight for their height at the time of death had more Alzheimer brain changes at autopsy, this is the first study to show that lower weight up to 10 years earlier is specifically related to the severity of the disease. "While weight one year or less prior to death was related to the amount of cognitive decline, this association could be explained by the severity of the Alzheimer process in the brain seen at autopsy," said Dr. Mortimer, professor of epidemiology at the USF College of Public Health. "Given its very long duration prior to onset of dementia, it is likely that weight loss is specifically associated with the Alzheimer disease process and not to a restriction in food intake due to cognitive decline," he said. "There is considerable evidence that Alzheimer changes in the brain precede the first symptoms of this illness by decades." Unexplained weight loss late in life, when coupled with other biomarkers, may help to identify those at risk of Alzheimer's disease more than a decade in the future. Identification of individuals who are at high risk of Alzheimer's long before cognitive decline becomes evident will be critical to its prevention once agents become available to slow the disease, Dr. Mortimer said.
The Nun Study, begun in 1992, is a study of 678 Catholic sisters, initially 75 to 102 years of age, who are evaluated yearly and who agreed to brain donation at the time of death. The Nun Study is directed by Dr. David Snowdon of the University of Kentucky. Dr. Snowdon is a co-author of the presentation as is Dr. William Markesbery, director of the Sanders-Brown Center on Aging at the University of Kentucky. Dr. Yougui Wu, the third coauthor, is an assistant professor of epidemiology and biostatistics at the USF College of Public Health
The Nun Study is funded by a grant from the National Institute on Aging.

ABC 7 Medical: Alzheimer's Disease

WJLA, ABC7 Medical by Kathy Fowler (11 June 2007) - Washington, DC, USA: Tony Sudler, Alzheimer's Association: "We look for Alzheimer's disease as projecting to bankrupt both Medicaid and Medicare in the future if we cannot...

Anchor: Alzheimer's disease is being called this country's next public health crisis. The number of people sick with this devastating disease is expected to quadruple by 2050. experts worry it's an epidemic that could break the healthcare system. Medical reporter Kathy Fowler joins us with the story.

Researchers at Johns Hopkins project in 40 years more than 100 million people worldwide will have Alzheimer's. Tonight health experts are warning - this is a problem so big it could bankrupt the united states healthcare system.

Story:
Jerome Menefee's mother is 82 years old and in the late stages of Alzheimer's so he quit his job to become her 24 hour caregiver.

Jerome Menefee, caregiver: "When I was born I was two pounds 14 ounces in 1953, you know a preemie; i only survived because of her." He promised to take care of her the way she took care of him.... but it takes a physical and emotional toll.

Jerome Menefee: "it was exhausting... my health was suffering... if i get sick no one else is going to take care of her." Not to mention the financial burden.....

Jerome Menefee" i'm looking at the possibility of selling the house and then taking what's available after taxes into an annuity to give her another income stream and then i'll start over. "

Health experts say right now one in eight people over the age of 65 has Alzheimer's and one in two people get the disease over the age of 85.

That's not even considering the 78 million aging baby bommers.....

Tony Sudler, alzheimer's association: "we look for alzheimer's disease as projecting to bankrupt both medicaid and medicare in the future if we cannot figure out a way to slow the diseases down."

Scientists are scrambling to come up with better treatments and say this is exactly the wrong time for the government to cut research funding.

Dr. Sam Gandy, Farber Institute for Neurosciences: "Alzheimer's funding for the NIH fell for the first time in 30 years. so as the epidemic is upon us, it's becoming more and more difficult to retain good scientist in the field."
Kathy on set:

Scientists say they might be close - maybe three to five years away from developing medicines that can slow down and maybe even prevent alzheimer's.

In the meantime, doctors say everyone can protect their brains by exercising and reducing blood pressure and cholesterol. basically the same things that prevent heart disease can also prevent Alzheimer's.

Dimebon Shows Promise When Treating Alzheimer's Disease

Ecanadanow.com, 11 June 2007 -- Importantly, on every endpoint studied, the benefits of Dimebon over placebo at one year were stable or greater when compared to benefits at six months. Dimebon patients were stabilized over the one year study period, meaning that their level of function was preserved for a full year on all five endpoints. The endpoints spanned all of the most frequently studied aspects of Alzheimer's disease: cognition, overall clinical function, activities of daily living, and behavioral problems. Dimebon was well tolerated throughout the entire one-year treatment period.On the study's primary endpoint, the ADAS-cog, Dimebon caused an improvement over placebo of 6.9 points at one year (observed case analysis; p<0.0001). p="0.006)." p="0.006)." p="0.03)">

Heart Disease a Risk Factor for Alzheimer's

Alz.org press info by HealthDay News - SUNDAY, 10 June 2007 -- There's more evidence that cardiovascular problems help drive Alzheimer's disease, scientists say, and that treating the heart might help protect the brain. The findings "represent hope that interventions with well-known drugs can interfere with the disease's progression," said lead investigator Yan Deschaintre, a neurologist and research fellow at the University Regional Hospital Center in Lille, France. In fact, cognitive impairment, as measured by a standard test, stayed in the low end of the mild range over 36 months for Alzheimer's patients who got treatments for both the neurological disease and their cardiovascular problems, the researchers reported. In contrast, Alzheimer's patients with vascular trouble who did not receive these medications experienced declines in cognition that approached the severe level, Deschaintre's team found. They were slated to present the findings Sunday at the Alzheimer Association's International Conference on Prevention of Dementia, in Washington, D.C... The work done by Deschaintre's team is consistent "with what we've been hearing over the past three to five years" about vascular risk factors increasing the risk for Alzheimer's, Gandy said. The new study, "really nails that down by looking at the other side of the coin by establishing that treating vascular risk factors slows the progression of cognitive decline," he added. He suggested that physicians begin to take vascular risk factors seriously as they treat patients with Alzheimer's. The vascular risk factors for early Alzheimer's patients "certainly should be treated" because it "seems to slow progression," Gandy said. Another expert agreed. The Lille results "reinforce the treatment guidelines for these vascular conditions, such as hypertension and diabetes, and emphasize that Alzheimer's and demented patients should be treated, too," said Hugh C. Hendrie, a professor of psychiatry at the Indiana University Medical School and a scientist at its Center for Aging Research. However, Deschaintre and Hendrie both noted that physicians at times may not treat vascular risk factors in Alzheimer's patients, for a variety of reasons. For example, Alzheimer's disease often leaves patients apathetic, so they may neglect to tell their physicians about vascular symptoms, Hendrie said. And Deschaintre noted that, in the clinic where the research was done, patients with Alzheimer's were less likely than other patients to be treated for vascular risk factors. The reverse was true, as well -- patients with vascular dementia were more likely to be treated for heart risk factors, but not for Alzheimer's. But, "since the majority of patients have both Alzheimer's disease and cerebrovascular disease, and since patients with pure Alzheimer's do seem to benefit from treatment of vascular risk factors, the message is to treat both conditions rather than to focus only on one," he said. Hendrie remained cautious about the scientific impact of Deschaintre's study, however. He said results from a clinical epidemiological study, such as the Lille research, aren't as conclusive or compelling as those from randomized, controlled clinical trials. Two other studies scheduled for release at the Alzheimer's conference on Sunday also emphasized the role of the brain-body connection in cognitive impairment and dementia. Weight loss may signal the onset of Alzheimer's, and the rate of weight loss could be early warning of dementia severity, according to a new review of data from what's known as the Nun's Study. That effort followed health outcomes for a group of 537 non-demented Catholic sisters, aged 75 to 102, for 10 years. In the study, a team led by Dr. James Mortimer, a professor of epidemiology and biostatistics at the University of South Florida, Tampa, found that unexplained weight loss late in life was often linked to Alzheimer's neuropathology in the brain and not to any change in eating habits linked to Alzheimer's. Mortimer explained that, "early weight loss appears to result from the Alzheimer's disease process itself before that process leads to dementia. That's why it is a marker of impending dementia." In a third study, a team from the Mayo Clinic in Rochester, Minn., found an increased risk of mild cognitive impairment (MCI) or dementia among 70- to 89-year-olds who have had a carotid endarterectomy (surgical clearance of the carotid artery, which brings blood to the brain) or a stroke or "mini-stroke," also known as a transient ischemic attack (TIA). In the study, the team compared the medical histories of 295 people with MCI and 590 age and sex-matched controls. "Elderly subjects who have had a carotid endarterectomy or stroke or TIA are about two times more likely to have MCI," lead researcher Dr. Rosebud O. Roberts, a Mayo epidemiologist, said in a prepared statement.