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Abstract
Cultured muscle fibers (CMF) from a patient with inclusion-body myositis (IBM) and cardiac amyloidosis associated with the transthyretin (TTR) Val122Ile mutation contained aspects of the IBM phenotype: vacuolation, congophilic inclusions, and clusters of immunocolocalizing amyloid β-peptide (Aβ) and TTR accumulations. These abnormalities are never present in normal human CMF. These perturbations were greatly increased after Aβ precursor protein gene transfer. The TTR mutation may be a genetic predisposition factor for the patient’s IBM.
- Received December 19, 2002.
- Accepted March 25, 2003.
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