Sporadic inclusion body myositis (sIBM) is one of the most frequent acquired myopathy in middle and later life. sIBM is histologically characterized by combination of inflammation and degeneration as well as multiple protein deposits in the myofibers. Sarcoplasmic accumulation of TDP-43 was more frequently observed in sIBM. In addition, mitochondrial abnormality has been proposed as the possible pathomechanism. To comfirm the association between TDP-43 accumulation and mitochondrial dysfunction, we have generated muscle-specific wild-type TDP-43 transgenic mice using creatine kinase (CK8) promoter, and then analyzed the mitochondrial function in the mice.

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