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From the Department of Molecular Biology and Biochemistry, University of California, Irvine, CA.
Address correspondence and reprint requests to Dr. Charles G. Glabe, Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697; e-mail: cglabe{at}uci.edu
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.
This article was previously published in electronic format as an Expedited E-Pub at www.neurology.org.
Disclosure: C.G. and R.K. are consultants for Kinexis, Inc., receiving personal compensation in excess of $10,000/year.
Received June 22, 2005. Accepted in final form October 14, 2005.
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