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Alzheimer's Research Page
New Targets for Neurodegenerative Diseases: Autophagy and More
The first study reports the discovery of small molecules capable of
ameliorating the toxicity of aggregated huntingtin protein by
stimulating its clearance via autophagy. The work, from David
Rubinsztein and Cahir O’Kane from the University of Cambridge, England, and Stuart Schreiber at the Broad Institute of Harvard/MIT in the other Cambridge (Massachusetts), provides a first step toward the development of novel autophagy enhancers. Such compounds could provide a new therapeutic approach beyond polyglutamine diseases, to a range of neurodegenerative conditions where protein aggregation plays a role. The study appeared May 6 in the online edition of Nature Chemical Biology.
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The mysteries of the brain...  |
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Bea Gorman’s life story about living with familial Alzheimers.  |
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My research is focussed on the study of episodic memory in humans. I am particularly interested in how different brain regions, particularly those within the medial temporal lobe, contribute towards visual memory. More specifically, I am investigating whether the roles of different brain regions involved in memory can be delineated according to the category of stimulus to be remembered.
The Stanford/VA Alzheimer's Disease Research Center conducts leading research into the causes and treatment of Alzheimer's disease, a progressive disorder of the brain that affects approximately four million Americans. Read More...
Dr Michel Goedert - Our work has shown that the intraneuronal filaments found in these diseases are made of either microtubule-associated protein tau or alpha-synuclein. Mutations in the tau gene cause inherited forms of frontotemporal dementia and parkinsonism, whereas mutations in the alpha-synuclein gene cause familial forms of Parkinson's disease and dementia with Lewy bodies.
Popular pain and inflammation fighters like aspirin and Aleve, promoted as a possible preventive against Alzheimer’s disease, did nothing to stave off dementia or memory loss in those who took them, two new studies show. In one study, published in the medical journal Neurology, the over-the-counter remedy naproxen (Aleve, Naprosyn) and the prescription pain reliever celecoxib (Celebrex) did nothing to prevent Alzheimer’s disease. The other study, from the British Medical Journal, found that aspirin did nothing to prevent memory loss in older women. Read More...
(PHILADELPHIA) – Researchers at the University of Pennsylvania School of Medicine have shown that impaired function and loss of synapses in the hippocampus of a mouse form of Alzheimer’s disease (AD) is related to the activation of immune cells called microglia, which cause inflammation. These events precede the formation of tangles – twisted fibers of tau protein that build up inside nerve cells – a hallmark of advanced AD. The researchers report their findings in the February 1 issue of Neuron. Research Advances at NIHThe National Institute on Aging (NIA), part of the Federal Government’s National Institutes of Health (NIH), has primary responsibility for basic research in Alzheimer’s disease (AD) as well as research aimed at finding ways to prevent and treat AD. The Institute’s AD research program is integral to one of its main goals, which is to enhance the quality of life of older people by expanding knowledge about the aging brain and nervous system. This 2004-2005 Progress Report on Alzheimer’s Disease summarizes recent AD research conducted or supported by NIA
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