Abstract
Biochemical and genetic investigations have identified four key proteins, mutations in which either cause Alzheimer disease (AD) (beta-amyloid precursor protein, presenilin 1 and 2) or confer a higher risk of developing AD (apolipoprotein E). This paper discusses the biochemical evidence that links each protein to AD, various animal and cell models that have been used in these investigations, and the putative interactions between these proteins that lead to AD. Areas that are especially fertile for novel research are noted as are gaps in our present understanding of the etiology of AD.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Aged
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Alzheimer Disease / genetics*
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Alzheimer Disease / metabolism*
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Amyloid beta-Protein Precursor / genetics
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Amyloid beta-Protein Precursor / metabolism
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Animals
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Apolipoproteins E / genetics
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Apolipoproteins E / metabolism
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Biochemistry / trends*
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Disease Models, Animal
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Humans
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Membrane Proteins / genetics
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Membrane Proteins / metabolism
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Molecular Biology / trends*
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Nerve Degeneration / genetics
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Nerve Degeneration / metabolism
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Research / trends
Substances
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Amyloid beta-Protein Precursor
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Apolipoproteins E
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Membrane Proteins