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2006 Grant - Van Nostrand
Inhibition of A-Beta Fibrillogenesis by Myelin Basic Protein
William Van Nostrand, Ph.D.
The Research Foundation of SUNY
State University of New York
Stony Brook, New York
2006 Investigator-Initiated Research Grant
Beta-amyloid protein fragments, key suspects in Alzheimer pathology, assemble themselves into small clusters, which, in turn, form strand-like structures called fibrils. Fibrils form larger structures that eventually form the hallmark amyloid plaques of Alzheimer's disease. Amyloid plaques form in the spaces between brain cells.
Deposits of amyloid fibril-based structures may also occur in blood vessels in the Alzheimer brain. While this is not a defining characteristic of Alzheimer's disease, it is the defining characteristic of a disorder called cerebral amyloid angiopathy (CAA). Differences and similarities between the two disorders can provide some clues about pathological processes at work in both of them.
William Van Nostrand, Ph.D., and colleagues are examining why people with certain inherited forms of CAA have the characteristic amyloid deposits in brain blood vessels but very few amyloid deposits among brain cells. They have hypothesized that the brain may contain factors that inhibit fibril formation of CAA-specific beta-amyloid.
The researchers recently observed that a brain protein called myelin basic protein binds to CAA-specific beta-amyloid and impedes its assembly into fibrils. In this study, they will characterize the interaction of these proteins and determine the mechanism of action that impedes fibril formation. This work may provide important insight into a factor that may affect the extent and location of beta-amyloid assembly in Alzheimer's disease, CAA and related brain disorders.