Transfer of β-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle

摘要

As in Alzheimer-disease (AD) brain, vacuo- lated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumulated β-amyloid precursor protein (βAPP), including its β-amyloid protein epitope, and in- creased βAPP-751 mRNA. Other similarities between IBM muscle and AD brain phenotypes include paired helical fila ments, hyperphosphorylated tau protein, apolipoprotein E, and mitochondrial abnormalities, including decreased cyto- chrome-c oxidase (COX) activity. The pathogenesis of these abnormalities in IBM muscle and AD brain is not known.