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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers.

Myostatin is a negative regulator of muscle mass and strength. Sporadic inclusion-body myositis (s-IBM) is the most common degenerative muscle disease of older persons and is characterized by pronounced muscle wasting. s-IBM is of unknown etiology and pathogenesis, and it lacks definitive treatment. We have now demonstrated in samples from 12 s-IBM biopsies that: (1) by light and electron microscopic immunocytochemistry, myostatin/myostatin precursor is accumulated within muscle fibers and co-localized with amyloid-beta (Abeta); (2) by immunoblots, both myostatin and myostatin precursor are increased; and (3) by immunoprecipitation, myostatin precursor complexes with Abeta. Our study suggests that myostatin/myostatin precursor, either alone, or bound to Abeta, may play a novel role in the pathogenesis of s-IBM.[1]

References

  1. Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers. Wójcik, S., Engel, W.K., McFerrin, J., Askanas, V. Acta Neuropathol. (2005) [Pubmed]
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