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Brain and brawn

Parallels in oxidative strength

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.

Address correspondence and reprint requests to Dr. George Perry, Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106; e-mail: george.perry{at}case.edu

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-β deposition and hyperphosphorylated function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative damage. Amyloid-β and 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.

This article was previously published in electronic format as an Expedited E-Pub at www.neurology.org.

Supported by the National Institues of Health, the Alzheimer's Association, Philip Morris USA Inc., and Philip Morris International.

Disclosure: The authors report no conflicts of interest.

Received June 22, 2005. Accepted in final form October 14, 2005.

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