Abstract
Recent findings indicate that soluble amyloid oligomers may represent the primary pathologic species in degenerative diseases. These amyloid oligomers share common structural features and the ability to permeabilize membranes, suggesting that they also share a common primary mechanism of pathogenesis. Membrane permeabilization by amyloid oligomers may initiate a common group of downstream pathologic processes, including intracellular calcium dyshomeostasis, production of reactive oxygen species, altered signaling pathways, and mitochondrial dysfunction that represent key effectors of cellular dysfunction and cell death in amyloid-associated degenerative disease, such as sporadic inclusion-body myositis.
MeSH terms
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Alzheimer Disease / etiology
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Alzheimer Disease / metabolism
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Amyloid / chemistry
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Amyloid / metabolism*
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Amyloid beta-Peptides / immunology
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Amyloidosis / etiology
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Amyloidosis / metabolism
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Animals
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Antibody Specificity
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Biopolymers
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Calcium / metabolism
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Cell Membrane Permeability
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Dementia / etiology
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Dementia / metabolism
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Drug Design
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Humans
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Huntington Disease / etiology
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Huntington Disease / metabolism
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Inclusion Bodies / chemistry
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Mice
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Mice, Transgenic
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Mitochondria / physiology
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Myositis, Inclusion Body / etiology
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Myositis, Inclusion Body / metabolism
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Parkinson Disease / etiology
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Parkinson Disease / metabolism
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Protein Folding
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Reactive Oxygen Species / metabolism
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Signal Transduction
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Solubility
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Structure-Activity Relationship
Substances
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Amyloid
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Amyloid beta-Peptides
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Biopolymers
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Reactive Oxygen Species
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Calcium