Abstract
The amyloid cascade hypothesis postulates that accumulation of beta-amyloid (Abeta) plays a key role in the development of Alzheimer's disease (AD). Accordingly, much effort has gone into reducing the amyloid burden, especially in transgenic mice expressing mutations in human amyloid precursor protein. Such mice develop amyloid plaques but not neurofibrillary tangles. Immunization with Abeta and other inflammatory stimuli, inhibitors of Abeta formation, cholesterol lowering agents, beta-sheet breaker peptides, antioxidants and various miscellaneous agents have been found to reduce the more soluble Abeta in such transgenic mice. Whether they would affect the more consolidated, cross-linked Abeta of AD and, if they did, whether that would really prove an effective treatment for the disease remains for future research to determine.
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