Key result
Beta-amyloid precursor protein overexpression is postulated to trigger the early pathogenic cascade in inclusion-body myopathies.
Population
Patients with sporadic inclusion-body myositis (s-IBM) and hereditary inclusion-body myopathy (h-IBM)
Design
Review
Authors
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No immediate change to IBM care; leaves open APP as upstream target pending validation studies.
This review highlights the shared pathologic features between s-IBM and h-IBM, proposing beta-amyloid precursor protein overexpression as a key early pathogenic event with parallels to Alzheimer's disease.
Askanas et al. (1998) conducted a review in Sporadic inclusion-body myositis (s-IBM) and hereditary inclusion-body myopathy (h-IBM). Overexpression of beta-amyloid precursor protein within abnormal muscle fibers is postulated as an early upstream event causing the pathogenic cascade in inclusion-body myositis and myopathies.
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