Plaque busters: strategies to inhibit amyloid formation in Alzheimer's disease

被引:126
作者
Soto, C
机构
[1] Unniversity of Chile, Dept of Biology, Faculty of Sciences
[2] Serono Pharmacutical Researche Institute, Ouates Geneva
来源
MOLECULAR MEDICINE TODAY | 1999年 / 5卷 / 08期
关键词
D O I
10.1016/S1357-4310(99)01508-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alzheimer's disease is a devastating degenerative disorder of the brain for which there is no cure or effective treatment. Although the etiology of Alzheimer's disease is not fully understood, recent research suggests that deposition of cerebral amyloid plaques is central to the disease process. Therefore, an attractive therapeutic strategy for Alzheimer's disease is to prevent, reduce or reverse amyloid deposition in the brain. Several small chemical compounds, synthetic peptides and natural proteins have been described that inhibit amyloid formation or amyloid neurotoxicity in vitro. The effect of these and other compounds now needs to be tested in vivo and the ability of amyloid inhibitors to halt the progression of Alzheimer's disease in humans needs to be evaluated.
引用
收藏
页码:343 / 350
页数:8
相关论文
共 52 条
[11]   Animal models of Alzheimer's disease [J].
Higgins, LS .
MOLECULAR MEDICINE TODAY, 1999, 5 (06) :274-276
[12]   SUBSTITUTIONS OF HYDROPHOBIC AMINO-ACIDS REDUCE THE AMYLOIDOGENICITY OF ALZHEIMERS-DISEASE BETA-A4 PEPTIDES [J].
HILBICH, C ;
KISTERSWOIKE, B ;
REED, J ;
MASTERS, CL ;
BEYREUTHER, K .
JOURNAL OF MOLECULAR BIOLOGY, 1992, 228 (02) :460-473
[13]   THE CARBOXY TERMINUS OF THE BETA-AMYLOID PROTEIN IS CRITICAL FOR THE SEEDING OF AMYLOID FORMATION - IMPLICATIONS FOR THE PATHOGENESIS OF ALZHEIMERS-DISEASE [J].
JARRETT, JT ;
BERGER, EP ;
LANSBURY, PT .
BIOCHEMISTRY, 1993, 32 (18) :4693-4697
[14]   Alternative conformations of amyloidogenic proteins govern their behavior [J].
Kelly, JW .
CURRENT OPINION IN STRUCTURAL BIOLOGY, 1996, 6 (01) :11-17
[15]   ARRESTING AMYLOIDOSIS IN-VIVO USING SMALL-MOLECULE ANIONIC SULFONATES OR SULFATES - IMPLICATIONS FOR ALZHEIMERS-DISEASE [J].
KISILEVSKY, R ;
LEMIEUX, LJ ;
FRASER, PE ;
KONG, XQ ;
HULTIN, PG ;
SZAREK, WA .
NATURE MEDICINE, 1995, 1 (02) :143-148
[16]   H-1-NMR OF A-BETA AMYLOID PEPTIDE CONGENERS IN WATER SOLUTION - CONFORMATIONAL-CHANGES CORRELATE WITH PLAQUE COMPETENCE [J].
LEE, JP ;
STIMSON, ER ;
GHILARDI, JR ;
MANTYH, PW ;
LU, YA ;
FELIX, AM ;
LLANOS, W ;
BEHBIN, A ;
CUMMINGS, M ;
VANCRIEKINGE, M ;
TIMMS, W ;
MAGGIO, JE .
BIOCHEMISTRY, 1995, 34 (15) :5191-5200
[17]   BETA-AMYLOID NEUROTOXICITY REQUIRES FIBRIL FORMATION AND IS INHIBITED BY CONGO RED [J].
LORENZO, A ;
YANKNER, BA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (25) :12243-12247
[18]   Brain amyloid - A physicochemical perspective [J].
Maggio, JE ;
Mantyh, PW .
BRAIN PATHOLOGY, 1996, 6 (02) :147-162
[20]   INTERACTION OF THE ANTHRACYCLINE 4'-IODO-4'-DEOXYDOXORUBICIN WITH AMYLOID FIBRILS - INHIBITION OF AMYLOIDOGENESIS [J].
MERLINI, G ;
ASCARI, E ;
AMBOLDI, N ;
BELLOTTI, V ;
ARBUSTINI, E ;
PERFETTI, V ;
FERRARI, M ;
ZORZOLI, I ;
MARINONE, MG ;
GARINI, P ;
DIEGOLI, M ;
TRIZIO, D ;
BALLINARI, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (07) :2959-2963