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Published online before print December 16, 2005, doi:10.1212/01.wnl.0000192259.34541.e4)
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NEUROLOGY 2006;66:S1-S6
© 2006 American Academy of Neurology

A perspective on sporadic inclusion-body myositis

The role of aging and inflammatory processes

Caleb E. Finch, PhD

From the Andrus Gerontology Center, Department of Biological Sciences, University of Southern California, Los Angeles, CA.

Address correspondence and reprint requests to Dr. Caleb E. Finch, Andrus Gerontology Center, Department of Biological Sciences, University of Southern California, 3715 McClintock, Los Angeles, CA 90089-0191; e-mail: cefinch{at}usc.edu

Sporadic inclusion-body myositis (sIBM) is an age-related condition manifested after midlife. This review points out salient features of sIBM that are shared with normal aging in muscle and with inflammatory changes in vascular atheromas and senile plaques of Alzheimer disease (AD). The amyloid precursor protein (APP) and derived Abeta peptides are found in both AD and sIBM. Because transgenic expression of human APP induces sIBM like changes, it is of potential interest that an inducer of APP, IL-1, increases during aging in mouse muscle. Because various subsets of the usual aging changes in aging brain, muscle, and vessels can be attenuated in rodents by caloric intake and possibly in humans by drugs with anti-inflammatory and anticoagulant activities, this study suggests that diet and inflammation may be useful experimental variations in exploring the pathogenesis of sIBM.

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

Supported by the Alzheimer’s Association, by the John Douglas French Alzheimer’s Foundation, and by the National Institute on Aging (AG13499).

Disclosure: The author is co-founder and major stockholder of Acumen Pharmaceuticals, which develops therapies for Alzheimer disease. The author reports no conflicts of interest.

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




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