TY - JOUR
T1 - Common structure and toxic function of amyloid oligomers implies a common mechanism of pathogenesis
AU - Glabe, Charles G.
AU - Kayed, Rakez
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2006/1
Y1 - 2006/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=33644861975&partnerID=8YFLogxK
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U2 - 10.1212/01.wnl.0000192103.24796.42
DO - 10.1212/01.wnl.0000192103.24796.42
M3 - Article
C2 - 16432151
AN - SCOPUS:33644861975
SN - 0028-3878
VL - 66
SP - S74-S78
JO - Neurology
JF - Neurology
IS - 2 SUPPL. 1
ER -