Abstract
Many neurodegenerative diseases are characterized by the progressive accumulation of aggregated protein. Recent evidence suggests the prion-like propagation of protein misfolding underlies the spread of pathology observed in these diseases. This review traces our understanding of the mechanisms that underlie this phenomenon and discusses related therapeutic strategies that derive from it.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Amyloid beta-Peptides
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Animals
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Brain / metabolism*
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Brain / pathology
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Humans
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Neurodegenerative Diseases / etiology
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Neurodegenerative Diseases / metabolism*
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Neurodegenerative Diseases / pathology*
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Neurons / metabolism
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Prions / metabolism*
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Protein Conformation
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alpha-Synuclein
Substances
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Amyloid beta-Peptides
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Prions
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alpha-Synuclein