Jennifer Raymond, an associate professor in neurobiology at Stanford University, is building a circuit diagram of the brain. By bridging the gap between individual synapses and whole brain learning and memory, her research is offering new insights and strategies for medical rehabilitation and education.
Amyloid Deposits in Cognitively Normal People May Predict Risk for Alzheimer’s Disease
December 14, 2009 | by
For people free of dementia, abnormal deposits of a protein associated with Alzheimer’s disease are associated with increased risk of developing the symptoms of the progressive brain disorder, according to two studies from researchers at Washington University in St. Louis. The studies, primarily funded by the National Institute on Aging (NIA), part of the National Institutes of Health, linked higher amounts of the protein deposits in dementia-free people with greater risk for developing the disease, and with loss of brain volume and subtle declines in cognitive abilities.
Neurodegenerative Disease and the Coming Epidemic
December 11, 2008 | by
At Neuroscience 2008, the 38th annual meeting of the Society for Neuroscience held last month in Washington D.C., a number of researchers presented evidence that a small, soluble, clustered form of a protein called amyloid beta may be responsible for brain damage in Alzheimer’s disease patients [1]. In addition, scientists report that they are finding new sources and uses of neural stem cells that may replace cells damaged by neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease [2].
Why are these reports significant? Because until recently, large insoluble amyloid beta plaques, or deposits, were considered the likely cause of Alzheimer’s disease. The plaques were thought to disrupt brain cell communication. However, new findings show that an early (i.e. small), soluble, clustered form of amyloid beta called protofibrils is found in high levels in the brains of people with Alzheimer’s disease [1]. Researchers also found a strong correlation between the presence of high levels of protofibrils in the brains of transgenic mouse models of Alzheimer’s disease and the cognitive impairments associated with the disease.
