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.
