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Titolo:
Apolipoprotein J (clusterin) and Alzheimer's disease
Autore:
Calero, M; Rostagno, A; Matsubara, E; Zlokovic, B; Frangione, B; Ghiso, J;
Indirizzi:
NYU, Sch Med, Dept Pathol, New York, NY 10016 USA NYU New York NY USA 10016 U, Sch Med, Dept Pathol, New York, NY 10016 USA Gunma Univ, Sch Med, Dept Neurol, Maebashi, Gumma 3718511, Japan Gunma Univ Maebashi Gumma Japan 3718511 l, Maebashi, Gumma 3718511, Japan Univ So Calif, Sch Med, Dept Neurol Surg, Los Angeles, CA 90089 USA Univ So Calif Los Angeles CA USA 90089 ol Surg, Los Angeles, CA 90089 USA
Titolo Testata:
MICROSCOPY RESEARCH AND TECHNIQUE
fascicolo: 4, volume: 50, anno: 2000,
pagine: 305 - 315
SICI:
1059-910X(20000815)50:4<305:AJ(AAD>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID-BETA-PEPTIDE; BLOOD-BRAIN-BARRIER; HUMAN CEREBROSPINAL-FLUID; SULFATED GLYCOPROTEIN-2 CLUSTERIN; HIGH-DENSITY-LIPOPROTEINS; ISOFORM-SPECIFIC BINDING; MEMBRANE-ATTACK COMPLEX; CENTRAL-NERVOUS-SYSTEM; RETE TESTIS FLUID; MESSENGER-RNA;
Keywords:
apolipoprotein J; soluble A beta; AD;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
120
Recensione:
Indirizzi per estratti:
Indirizzo: Ghiso, J NYU, Sch Med, Dept Pathol, 550 1st Ave,TH432, New York, NY 10016 USA NYU 550 1st Ave,TH432 New York NY USA 10016 ew York, NY 10016 USA
Citazione:
M. Calero et al., "Apolipoprotein J (clusterin) and Alzheimer's disease", MICROSC RES, 50(4), 2000, pp. 305-315

Abstract

Apolipoprotein J (clusterin) is a ubiquitous multifunctional glycoprotein capable of interacting with a broad spectrum of molecules. In pathological conditions, it is an amyloid associated protein, co-localizing with fibrillar deposits in systemic and localized amyloid disorders. In Alzheimer's disease, the most frequent form of amyloidosis in humans and the major cause of dementia in the elderly, apoJ is present in amyloid plaques and cerebrovascular deposits but is rarely seen in NFT-containing neurons. ApoJ expression is up-regulated in a wide variety of insults and may represent a defenseresponse against local damage to neurons. Four different mechanisms of action could be postulated to explain the role of apoJ as a neuroprotectant during cellular stress: (1) function as an anti-apoptotic signal, (2) protection against oxidative stress, (3) inhibition of the membrane attack complexof complement proteins locally activated as a result of inflammation, and (4) binding to hydrophobic regions of partially unfolded, stressed proteins, and therefore avoiding aggregation in a chaperone-like manner. This review focuses on the association of apoJ in biological fluids with Alzheimer's soluble AP. This interaction prevents Ap aggregation and fibrillization andmodulates its blood-brain barrier transport at the cerebrovascular endothelium. (C) 2000 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 13:25:45