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Titolo:
Sporadic inclusion-body myositis and its similarities to Alzheimer diseasebrain - Recent approaches to diagnosis and pathogenesis, and relation to aging
Autore:
Askanas, V; Engel, WK;
Indirizzi:
Univ So Calif, Sch Med, Dept Neurol, Good Samaritan Hosp,Neuromuscular Ctr, Univ So Calif Los Angeles CA USA 90033 Samaritan Hosp,Neuromuscular Ctr,
Titolo Testata:
SCANDINAVIAN JOURNAL OF RHEUMATOLOGY
fascicolo: 6, volume: 27, anno: 1998,
pagine: 389 - 405
SICI:
0300-9742(1998)27:6<389:SIMAIS>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
BETA-AMYLOID PRECURSOR; OCULOPHARYNGEAL MUSCULAR-DYSTROPHY; IDIOPATHIC INFLAMMATORY MYOPATHIES; PAIRED-HELICAL FILAMENTS; HUMAN NEUROMUSCULAR-JUNCTIONS; PROTEIN MESSENGER-RNA; APOLIPOPROTEIN-E; NEUROFIBRILLARY TANGLES; MUSCLE-FIBERS; PRION PROTEIN;
Keywords:
inclusion-body myositis; Alzheimer disease; aging; oxidative stress; beta-amyloid precursor protein;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
136
Recensione:
Indirizzi per estratti:
Indirizzo: Askanas, V USC Neuromuscular Ctr, 637 S Lucas Ave, Los Angeles, CA 90017 USA USC Neuromuscular Ctr 637 S Lucas Ave Los Angeles CA USA 90017
Citazione:
V. Askanas e W.K. Engel, "Sporadic inclusion-body myositis and its similarities to Alzheimer diseasebrain - Recent approaches to diagnosis and pathogenesis, and relation to aging", SC J RHEUM, 27(6), 1998, pp. 389-405

Abstract

Sporadic inclusion-body myositis (s-IBM) is the most common, debilitating and progressive muscle disease beginning at the age 50 or later. The most characteristic pathologic feature is vacuolar degeneration of muscle fibers accompanied by intrafiber congophilia and clusters ("tangles") of paired-helical filaments, containing phosphorylated tau. An unusual feature of sporadic inclusion-body myositis is accumulation within its abnormal muscle fibers of several proteins that are characteristic of Alzheimer disease brain, including epitopes of beta-amyloid precursor protein (beta APP), phosphorylated tau, alpha-l-antichymotrypsin, apolipoprotein E, and presenilin-1. Indicators of oxidative stress are also present within abnormal s-IBM muscle fibers. In this review, we describe new advances seeking the pathogenic mechanism of sporadic inclusion-body myositis. We hypothesize on the possible pathogenic role of abnormally accumulated proteins, and we propose that important contributory factors leading to inclusion-body myositis are the milieu of muscle-fiber aging and oxidative stress. In addition, we present evidence that overexpression of adenovirus-transferred beta APP gene in culturedhuman muscle fibers induces aspects of the inclusion-body myositis phenotype, and suggest that beta APP-overexpression is an early event in the pathogenic cascade causing inclusion-body myositis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 12:01:40