Design strategies for anti-amyloid agents

被引:114
作者
Mason, JM [1 ]
Kokkoni, N [1 ]
Stott, K [1 ]
Doig, AJ [1 ]
机构
[1] UMIST, Dept Biomol Sci, Senexis Ltd, Manchester M60 1QD, Lancs, England
基金
英国生物技术与生命科学研究理事会;
关键词
D O I
10.1016/S0959-440X(03)00100-3
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
Numerous diseases have been linked to a common pathogenic process called amyloidosis, whereby proteins or peptides clump together in the brain or body to form toxic soluble oligomers and/or insoluble fibres. An attractive strategy to develop therapies for these diseases is therefore to inhibit or reverse protein/peptide aggregation. A diverse range of small organic ligands have been found to act as aggregation inhibitors. Alternatively, the wild-type peptide can be derivatised so that it still binds to the amyloid target, but prevents further aggregation. This can be achieved by adding a bulky group or charged amino acid to either end of the peptide, or by incorporating proline residues or N-methylated amide groups.
引用
收藏
页码:526 / 532
页数:7
相关论文
共 54 条
[1]   Pharmacological profiles of peptide drug candidates for the treatment of Alzheimer's disease [J].
Adessi, C ;
Frossard, MJ ;
Boissard, C ;
Fraga, S ;
Bieler, S ;
Ruckle, T ;
Vilbois, F ;
Robinson, SM ;
Mutter, M ;
Banks, WA ;
Soto, C .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (16) :13905-13911
[2]   β-amyloid aggregation induced by human acetylcholinesterase:: inhibition studies [J].
Bartolini, M ;
Bertucci, C ;
Cavrini, V ;
Andrisano, V .
BIOCHEMICAL PHARMACOLOGY, 2003, 65 (03) :407-416
[3]   CONGO-RED PROTECTS AGAINST TOXICITY OF BETA-AMYLOID PEPTIDES ON RAT HIPPOCAMPAL-NEURONS [J].
BURGEVIN, MC ;
PASSAT, M ;
DANIEL, N ;
CAPET, M ;
DOBLE, A .
NEUROREPORT, 1994, 5 (18) :2429-2432
[4]   Metal complexing agents as therapies for Alzheimer's disease [J].
Bush, AI .
NEUROBIOLOGY OF AGING, 2002, 23 (06) :1031-1038
[5]   BETA-CYCLODEXTRIN INTERACTS WITH THE ALZHEIMER AMYLOID BETA-A4 PEPTIDE [J].
CAMILLERI, P ;
HASKINS, NJ ;
HOWLETT, DR .
FEBS LETTERS, 1994, 341 (2-3) :256-258
[6]  
CLARK A, 1987, LANCET, V2, P231
[7]   Emerging β-amyloid therapies for the treatment of Alzheimer's disease [J].
Conway, KA ;
Baxter, EW ;
Felsenstein, KM ;
Reitz, AB .
CURRENT PHARMACEUTICAL DESIGN, 2003, 9 (06) :427-447
[8]   β-amyloid production, aggregation, and clearance as targets for therapy in Alzheimer's disease [J].
De Felice, FG ;
Ferreira, ST .
CELLULAR AND MOLECULAR NEUROBIOLOGY, 2002, 22 (5-6) :545-563
[9]   Protein misfolding, evolution and disease [J].
Dobson, CM .
TRENDS IN BIOCHEMICAL SCIENCES, 1999, 24 (09) :329-332
[10]   Modified-peptide inhibitors of amyloid β-peptide polymerization [J].
Findeis, MA ;
Musso, GM ;
Arico-Muendel, CC ;
Benjamin, HW ;
Hundal, AM ;
Lee, JJ ;
Chin, J ;
Kelley, M ;
Wakefield, J ;
Hayward, NJ ;
Molineaux, SM .
BIOCHEMISTRY, 1999, 38 (21) :6791-6800