Abstract
One hundred years ago a small group of psychiatrists described the abnormal protein deposits in the brain that define the most common neurodegenerative diseases. Over the past 25 years, it has become clear that the proteins forming the deposits are central to the disease process. Amyloid-beta and tau make up the plaques and tangles of Alzheimer's disease, where these normally soluble proteins assemble into amyloid-like filaments. Tau inclusions are also found in a number of related disorders. Genetic studies have shown that dysfunction of amyloid-beta or tau is sufficient to cause dementia. The ongoing molecular dissection of the neurodegenerative pathways is expected to lead to a true understanding of disease pathogenesis.
Publication types
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Historical Article
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Alzheimer Disease* / genetics
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Alzheimer Disease* / history
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Alzheimer Disease* / metabolism
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Alzheimer Disease* / pathology
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Amyloid beta-Peptides / chemistry
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Amyloid beta-Peptides / 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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Brain / pathology
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Brain Chemistry
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History, 20th Century
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Humans
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Mutation
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Neurofibrillary Tangles / chemistry
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Neurofibrillary Tangles / pathology
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Plaque, Amyloid / chemistry
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Plaque, Amyloid / pathology
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Presenilin-1 / genetics
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Presenilin-1 / metabolism
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tau Proteins / chemistry
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tau Proteins / genetics
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tau Proteins / metabolism
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Apolipoproteins E
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Presenilin-1
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tau Proteins