Amyloidosis and Alzheimer's disease

被引：158

作者：

Ghiso, J ^{[1
]}

Frangione, B ^{[1
]}

机构：

[1] NYU, Sch Med, Dept Pathol & Psychiat, New York, NY 10016 USA

来源：

ADVANCED DRUG DELIVERY REVIEWS | 2002年 / 54卷 / 12期

关键词：

dementia; neurodegeneration; A beta; paired helical filaments; fibrillogenesis; familial Alzheimer's disease; A beta PP;

D O I：

10.1016/S0169-409X(02)00149-7

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Alzheimer's disease (AD) is the most frequent type of amyloidosis in humans and the commonest form of dementia. Extracellular Abeta amyloid deposits in the form of amyloid plaques and cerebral amyloid angiopathy as well as intraneuronal neurofibrillary tangles co-exist in the brain parenchyma of AD patients, the cognitive areas being the most severely affected. This review focuses on the potential role of amyloid in the development of neurodegeneration and presents studies of AD and other unrelated inherited dementia syndromes associated with neuronal loss and amyloid deposition in the brain. (C) 2002 Elsevier Science B.V. All rights reserved.

引用

页码：1539 / 1551

页数：13

共 84 条

[1] Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition [J].

Bales, KR ;

Verina, T ;

Dodel, RC ;

Du, YS ;

Altstiel, L ;

Bender, M ;

Hyslop, P ;

Johnstone, EM ;

Little, SP ;

Cummins, DJ ;

Piccardo, P ;

Ghetti, B ;

Paul, SM .

NATURE GENETICS, 1997, 17 (03) :263-264

[2] SKIN DEPOSITS IN HEREDITARY CYSTATIN-C AMYLOIDOSIS [J].

BENEDIKZ, E ;

BLONDAL, H ;

GUDMUNDSSON, G .

VIRCHOWS ARCHIV A-PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY, 1990, 417 (04) :325-331

[3]

BUGIANI O, 1998, NEUROBIOL AGING, V19, pS238

[4] EARLY-ONSET ALZHEIMERS-DISEASE CAUSED BY MUTATIONS AT CODON-717 OF THE BETA-AMYLOID PRECURSOR PROTEIN GENE [J].

CHARTIERHARLIN, MC ;

CRAWFORD, F ;

HOULDEN, H ;

WARREN, A ;

HUGHES, D ;

FIDANI, L ;

GOATE, A ;

ROSSOR, M ;

ROQUES, P ;

HARDY, J ;

MULLAN, M .

NATURE, 1991, 353 (6347) :844-846

[5] Presenilins: Multifunctional proteins involved in Alzheimer's disease pathology [J].

Checler, F .

IUBMB LIFE, 1999, 48 (01) :33-39

[6] Protein misfolding and prion diseases [J].

Cohen, FE .

JOURNAL OF MOLECULAR BIOLOGY, 1999, 293 (02) :313-320

[7] GENE DOSE OF APOLIPOPROTEIN-E TYPE-4 ALLELE AND THE RISK OF ALZHEIMERS-DISEASE IN LATE-ONSET FAMILIES [J].

CORDER, EH ;

SAUNDERS, AM ;

STRITTMATTER, WJ ;

SCHMECHEL, DE ;

GASKELL, PC ;

SMALL, GW ;

ROSES, AD ;

HAINES, JL ;

PERICAKVANCE, MA .

SCIENCE, 1993, 261 (5123) :921-923

[8] A polymorphism in the cystatin C gene is a novel risk factor for late-onset Alzheimer's disease [J].

Crawford, FC ;

Freeman, MJ ;

Schinka, JA ;

Abdullah, LI ;

Gold, M ;

Hartman, R ;

Krivian, K ;

Morris, MD ;

Richards, D ;

Duara, R ;

Anand, R ;

Mullan, MJ .

NEUROLOGY, 2000, 55 (06) :763-768

[9] Protein misfolding, evolution and disease [J].

Dobson, CM .

TRENDS IN BIOCHEMICAL SCIENCES, 1999, 24 (09) :329-332

[10] A new pathogenic mutation in the APP gene (1716V) increases the relative proportion of A beta 42(43) [J].

Eckman, CB ;

Mehta, ND ;

Crook, R ;

Pereztur, J ;

Prihar, G ;

Pfeiffer, E ;

GraffRadford, N ;

Hinder, P ;

Yager, D ;

Zenk, B ;

Refolo, LM ;

Prada, CM ;

Younkin, SG ;

Hutton, M ;

Hardy, J .

HUMAN MOLECULAR GENETICS, 1997, 6 (12) :2087-2089

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