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Published online before print December 16, 2005, doi:10.1212/01.wnl.0000192307.15103.83)
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Received ,
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Brain and brawn. Parallels in oxidative strength

P. I. Moreira MA, K. Honda MD, PhD, X. Zhu PhD, A. Nunomura MD, PhD, G. Casadesus PhD, M. A. Smith PhD, and G. Perry PhD*

From the Institute of Pathology (P.I.M., K.H., X.Z., G.C., M.A.S., G.P.), Case Western Reserve University, Cleveland, OH; the Center for Neuroscience and Cell Biology of Coimbra (P.I.M.), University of Coimbra, Coimbra, Portugal; and the Department of Psychiatry and Neurology (A.N.), Asahikawa Medical College, Asahikawa, Japan.


* To whom correspondence should be addressed. E-mail: george.perry{at}case.edu.

Abstract--Neuronal oxidative stress occurs early in the progression of Alzheimer disease (AD), significantly before the development of the pathologic hallmarks, neurofibrillary tangles, and senile plaques. Study of Down syndrome, cases with autosomal dominant mutation, and sporadic AD all suggest amyloid-{beta} deposition and hyperphosphorylated {tau} function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative damage. Amyloid-{beta} and {tau} hyperphosphorylation also define vulnerable muscle cells in sporadic inclusion-body myositis (s-IBM). The role of the structural changes of s-IBM, as in AD, remains to be determined but may mark a critical response yielding a novel balance in oxidant homeostasis.




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