Physiopathological modulators of amyloid aggregation and novel pharmacological approaches in Alzheimer's disease

被引:17
作者
Defelice, FG [1 ]
Ferreira, ST [1 ]
机构
[1] Univ Fed Rio de Janeiro, Inst Biomed Sci, Dept Biochem Med, BR-21944590 Rio De Janeiro, Brazil
来源
ANAIS DA ACADEMIA BRASILEIRA DE CIENCIAS | 2002年 / 74卷 / 02期
关键词
Alzheimer's disease; A beta peptide; aggregation; neurotoxicity; physiopathological modulators;
D O I
10.1590/S0001-37652002000200006
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The biological mechanisms underlying the neuropathology of Alzheimer's disease (AD) are complex. as several factors likely contribute to the development of the disease, Therefore. it is not surprising that a number of different possible therapeutic approaches addressing distinct aspects of this disease are currently being investigated. Among these are ways to prevent amyloid aggregation and/or deposition. to prevent neuronal degeneration, and to increase brain neurotransmitter levels. Here, we discuss possible roles of endogenous modulators of Abeta aggregation in the physiopathology of AD and some of the strategies currently under consideration to interfere with brain levels of beta-amyloid, its aggregation and neurotoxicity.
引用
收藏
页码:265 / 284
页数:20
相关论文
共 161 条
[11]   Endogenous proteins controlling amyloid β-peptide polymerization -: Possible implications for β-amyloid formation in the central nervous system and in peripheral tissues [J].
Bohrmann, B ;
Tjernberg, L ;
Kuner, P ;
Poli, S ;
Levet-Trafit, B ;
Näslund, J ;
Richards, G ;
Huber, W ;
Döbeli, H ;
Nordstedt, C .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (23) :15990-15995
[12]   FERROUS IRON RELEASE FROM TRANSFERRIN BY HUMAN NEUTROPHIL-DERIVED SUPEROXIDE ANION - EFFECT OF PH AND IRON SATURATION [J].
BRIELAND, JK ;
FANTONE, JC .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1991, 284 (01) :78-83
[13]  
Brown AM, 1997, J NEUROCHEM, V69, P1204
[14]   PH-DEPENDENT BINDING OF SYNTHETIC BETA-AMYLOID PEPTIDES TO GLYCOSAMINOGLYCANS [J].
BRUNDEN, KR ;
RICHTERCOOK, NJ ;
CHATURVEDI, N ;
FREDERICKSON, RCA .
JOURNAL OF NEUROCHEMISTRY, 1993, 61 (06) :2147-2154
[15]   BINDING OF VASCULAR HEPARAN-SULFATE PROTEOGLYCAN TO ALZHEIMERS AMYLOID PRECURSOR PROTEIN IS MEDIATED IN PART BY THE N-TERMINAL REGION OF A4 PEPTIDE [J].
BUEE, L ;
DING, WH ;
ANDERSON, JP ;
NARINDRASORASAK, S ;
KISILEVSKY, R ;
BOYLE, NJ ;
ROBAKIS, NK ;
DELACOURTE, A ;
GREENBERG, B ;
FILLIT, HM .
BRAIN RESEARCH, 1993, 627 (02) :199-204
[16]   BINDING OF SECRETED HUMAN NEUROBLASTOMA PROTEOGLYCANS TO THE ALZHEIMERS AMYLOID A4 PEPTIDE [J].
BUEE, L ;
DING, W ;
DELACOURTE, A ;
FILLIT, H .
BRAIN RESEARCH, 1993, 601 (1-2) :154-163
[17]   RAPID INDUCTION OF ALZHEIMER A-BETA AMYLOID FORMATION BY ZINC [J].
BUSH, AI ;
PETTINGELL, WH ;
MULTHAUP, G ;
PARADIS, MD ;
VONSATTEL, JP ;
GUSELLA, JF ;
BEYREUTHER, K ;
MASTERS, CL ;
TANZI, RE .
SCIENCE, 1994, 265 (5177) :1464-1467
[18]   The sulfate moieties of glycosaminoglycans are critical for the enhancement of β-amyloid protein fibril formation [J].
Castillo, GM ;
Lukito, W ;
Wight, TN ;
Snow, AD .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (04) :1681-1687
[19]  
Castillo GM, 1997, J NEUROCHEM, V69, P2452
[20]   Chelation and intercalation: Complementary properties in a compound for the treatment of Alzheimer's disease [J].
Cherny, RA ;
Barnham, KJ ;
Lynch, T ;
Volitakis, I ;
Li, QX ;
McLean, CA ;
Multhaup, G ;
Beyreuher, K ;
Tanzi, RE ;
Masters, CL ;
Bush, AI .
JOURNAL OF STRUCTURAL BIOLOGY, 2000, 130 (2-3) :209-216