Study: Ginkgo doesn't cut dementia risk

edition.cnn.com — The popular herb ginkgo biloba does not reduce the risk of dementia or Alzheimer's disease, according to a study of more than 1,500 elderly patients who took the supplement. Often touted as a way to preserve aging memories, no large-scale, randomized clinical trial -- until now -- has thoroughly evaluated the safety and effectiveness of ginkgo biloba extract as a way to prevent dementia. In the new government-funded study, volunteers ages 75 and older with either normal mental function or mild cognitive impairment took a twice-daily placebo or ginkgo biloba extract (for a total of 240 milligrams per day). The researchers tested the volunteers' memory and other mental abilities every six months for about six years. Ginkgo supplements were no better than a placebo for preventing dementia, according to the study, which was sponsored by the National Center for Complementary and Alternative Medicine and the National Institute on Aging of the National Institutes of Health. It appears in the November 19 issue of the Journal of the American Medical Association. read more...

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More Alzheimer’s Risk for Hispanics, Studies Suggest

nytimes.com — He lost his job at a Queens bakery because he kept burning chocolate chip cookies, forgetting he had put them in the oven. Then he got lost going to job interviews, walking his neighborhood in circles. Teresa Mojica of Philadelphia was 59 when she got Alzheimer’s, making her so argumentative and delusional that she sometimes hits her husband. And Ida J. Lawrence was 57 when she started misplacing things and making mistakes in her Boston dental school job. read more...

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Tracking Alzheimer's-linked protein in live brains

news.yahoo.com — Scientists for the first time have peered into people's brains to directly measure the ebb and flow of a substance notorious for its role in Alzheimer's disease. The delicate research was performed not with Alzheimer's patients but with people suffering severe brain injuries — because a brain injury increases the risk of developing dementia later in life. read more...

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Promising New Drug Development Announced at Alzheimer’s Conference

healthnews.com — The 2008 International Conference on Alzheimer's Disease (ICAD) is taking place this week, July 26-31, at McCormick Place in Chicago. More than 5,000 world-renowned researchers from 60 countries were expected to be on hand for what is considered the world's largest gathering of international leaders in Alzheimer research and care ever convened. Through the sharing of information and resources on the cause, diagnosis, treatment and prevention of Alzheimer's and related disorders, new knowledge is generated and the research community is broadened. read more...

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'Biomarkers' May Help Spot, Track Alzheimer's

nlm.nih.gov — A biomarker -- something that can be measured and that gives an indication of what's going on inside the body -- will help in early detection, in testing new therapies and, once doctors have better drugs for Alzheimer's, with earlier intervention in the disease process. "If we're going to have any kind of medication that alters or modifies the disease, if it's really going to change it rather than treat symptoms, then we need biomarkers that are sensitive to the illness before a person becomes impaired," explained Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York City. "In Alzheimer's, we need two things: We need to know who's sick and who's not and, secondly, biomarkers should be treatment-sensitive, meaning if you've got the right treatment, you watch the biomarker go down, like blood sugar and insulin. That's the model we want." read more...

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Calcium May Be The Key To Understanding Alzheimer's Disease

sciencedaily.com — “The ‘calcium dysregulation’ hypothesis for inherited, early onset familial Alzheimer's disease has been suggested by previous research findings, but our current study identifies a molecular mechanism that makes this hypothesis very compelling,” says lead author J. Kevin Foskett, PhD, Professor of Physiology. “Mutated PS1 and PS2 caused exaggerated cellular calcium signaling in cells through a calcium channel in the endoplasmic reticulum called the inositol trisphosphate receptor [InsP3R], suggesting that it or other proteins in this calcium signaling pathway could be targets for new Alzheimer’s disease therapies.” The study appeared in the June 26 issue of Neuron. Alzheimer’s disease affects as many as 5 million Americans, 5 percent of whom have the familial form. The hallmark of the disease is the accumulation of tangles and plaques of amyloid beta protein in the brain. “The amyloid hypothesis has long been invoked to explain the cause of Alzheimer’s” says Foskett. In the Neuron study, cells that carried the disease-causing mutated form of PS1 showed increased processing of amyloid beta that depended on the interaction of the PS proteins with the InsP3R. This observation links mis-regulation of calcium inside cells with the production of amyloid, a characteristic feature in the brains of people with Alzheimer’s disease. This research was supported by grants from the National Institutes of Health and the Alzheimer's Disease Core Center at Penn. read more...

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Alzheimer's Drug Shows Early Promise

nlm.nih.gov — FRIDAY, June 27 (HealthDay News) -- Long-anticipated results from a trial on an experimental Alzheimer's therapy look promising, at least in a certain group of patients. Findings that are slated to be presented Sunday at the International Conference on Alzheimer's Disease in Chicago suggest that while the drug, bapineuzumab, showed only a modest trend towards a benefit in patients with the ApoE4 gene, there were more notable improvements in the degree of cognitive decline in individuals lacking the gene. Patients who lack the ApoE4 gene have a predisposition to developing Alzheimer's, especially earlier in life. "This is the first study of adequate size and duration that suggests the immunotherapy beta-amyloid model works," said Dr. Anton Porsteinsson, an associate professor of psychiatry at the University of Rochester School of Medicine who was one of the investigators for the study. "Immunotherapy is a huge front in the development of treatments." read more...

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Scientists Isolate a Toxic Key to Alzheimer's Disease in Human Brains

nih.gov — cientists have long questioned whether the abundant amounts of amyloid plaques found in the brains of patients with Alzheimer's actually caused the neurological disease or were a by-product of its progress. Now, using new research techniques, scientists have shown that a two-molecule aggregate (or dimer) of beta-amyloid protein fragments may play a role in initiating the disease. The study, supported by the National Institutes of Health, suggests a possible new target for developing drug therapies to combat the irreversible and progressive disorder. Ganesh M. Shankar, Ph.D., and Dennis J. Selkoe, M.D., of Brigham and Women's Hospital and Harvard Medical School, conducted the study in collaboration with other researchers at Harvard and in Ireland at University College Dublin, Beaumont Hospital and Royal College of Surgeons Ireland, and Trinity College Dublin. The National Institute on Aging (NIA), part of NIH, funded the study which appears online in the June 22, 2008, Nature Medicine. Alzheimer's disease is marked by the build-up of plaques consisting of beta-amyloid protein fragments, as well as abnormal tangles of tau protein found inside brain cells. Early in the disease, Alzheimer's pathology is first observed in the hippocampus, the part of the brain important to memory, and gradually spreads to the cerebral cortex, the outer layer of the brain. In this study, researchers tested cerebral cortex extracts from brains donated for autopsy by people aged 65 and older with Alzheimer's and other dementias, as well as those without dementia. The extracts contained soluble one-molecule (monomer), two-molecule (dimer), three-molecule (trimer) or larger aggregates of beta-amyloid, as well as insoluble plaque cores. The researchers then injected the extracts into normal rats or added the extracts to slices of normal mouse hippocampus. Shankar, Selkoe and colleagues discovered that both the soluble monomers and the insoluble plaque cores had no detectable effect on the hyppocampal slices. However, the soluble dimers induced certain key characteristics of Alzheimer's in the rats. The dimers impaired memory function, specifically the memories of newly learned behaviors. In the mouse hippocampal slices, the dimers also reduced by 47 percent the density of the dendrite spines that receive messages sent by other brain cells. The dimers seemed to be directly acting on synapses, the connections between neurons that are essential for communication between them. read more...

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