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, 153 (6), 1673-7

Does Overexpression of betaAPP in Aging Muscle Have a Pathogenic Role and a Relevance to Alzheimer's Disease? Clues From Inclusion Body Myositis, Cultured Human Muscle, and Transgenic Mice

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Does Overexpression of betaAPP in Aging Muscle Have a Pathogenic Role and a Relevance to Alzheimer's Disease? Clues From Inclusion Body Myositis, Cultured Human Muscle, and Transgenic Mice

V Askanas et al. Am J Pathol.

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Figure 1.
Figure 1.
Genetic defects in h-IBM and various factors (including a putative virus) in s-IBM lead to presently unknown mechanisms [“?” box in diagram]. These up-regulate βAPP transcription, resulting in βAPP overexpression. In the milieu of aging muscle of s-IBM or of adult muscle of h-IBM, overexpression producing excessive βAPP (the whole molecule or its Aβ fragment) leads to oxidative stress with increased free radicals, which contribute to producing the demonstrated IBM muscle fiber abnormalities. Those abnormalities are either directly associated with oxidative stress or possibly caused by oxidative stress. Perhaps some of the former contribute to producing, directly or indirectly, some of the latter. *, present in virtually all s-IBM patients and in the older h-IBM patients; **, both mRNA.

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