Recent work on Alzheimer's disease transgenics

被引：15

作者：

Duff, K ^{[1
]}

机构：

[1] Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA

来源：

CURRENT OPINION IN BIOTECHNOLOGY | 1998年 / 9卷 / 06期

关键词：

D O I：

10.1016/S0958-1669(98)80132-8

中图分类号：

Q5 [生物化学];

学科分类号：

071010 ; 081704 ;

摘要：

The most significant feature of the current transgenic models of Alzheimer's disease continues to be the amyloid phenotype. In the past year, mice have been more extensively characterized in terms of the effect of amyloid accumulation on downstream events, such as neurodegeneration and behavioral changes, but the results have been complex. Genetic crosses have shown that apolipoprotein E and TGF-beta 1 influence the deposition event and that the presenilins act synergistically with the amyloid precursor protein in pathology development. The mice have great utility in amyloid modulation studies but are still not complete models of Alzheimer's disease.

引用

页码：561 / 564

页数：4

共 27 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] Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins [J].

Borchelt, DR ;

Ratovitski, T ;

vanLare, J ;

Lee, MK ;

Gonzales, V ;

Jenkins, NA ;

Copeland, NG ;

Price, DL ;

Sisodia, SS .

NEURON, 1997, 19 (04) :939-945

[3] Familial Alzheimer's disease-linked presenilin 1 variants elevate A beta 1-42/1-40 ratio in vitro and in vivo [J].

Borchelt, DR ;

Thinakaran, G ;

Eckman, CB ;

Lee, MK ;

Davenport, F ;

Ratovitsky, T ;

Prada, CM ;

Kim, G ;

Seekins, S ;

Yager, D ;

Slunt, HH ;

Wang, R ;

Seeger, M ;

Levey, AI ;

Gandy, SE ;

Copeland, NG ;

Jenkins, NA ;

Price, DL ;

Younkin, SG .

NEURON, 1996, 17 (05) :1005-1013

[4] Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice [J].

Citron, M ;

Westaway, D ;

Xia, WM ;

Carlson, G ;

Diehl, T ;

Levesque, G ;

JohnsonWood, K ;

Lee, M ;

Seubert, P ;

Davis, A ;

Kholodenko, D ;

Motter, R ;

Sherrington, R ;

Perry, B ;

Yao, H ;

Strome, R ;

Lieberburg, I ;

Rommens, J ;

Kim, S ;

Schenk, D ;

Fraser, P ;

Hyslop, PS ;

Selkoe, DJ .

NATURE MEDICINE, 1997, 3 (01) :67-72

[5]

CONLON RA, 1995, DEVELOPMENT, V121, P1533

[6] PROTECTIVE EFFECT OF APOLIPOPROTEIN-E TYPE-2 ALLELE FOR LATE-ONSET ALZHEIMER-DISEASE [J].

CORDER, EH ;

SAUNDERS, AM ;

RISCH, NJ ;

STRITTMATTER, WJ ;

SCHMECHEL, DE ;

GASKELL, PC ;

RIMMLER, JB ;

LOCKE, PA ;

CONNEALLY, PM ;

SCHMADER, KE ;

SMALL, GW ;

ROSES, AD ;

HAINES, JL ;

PERICAKVANCE, MA .

NATURE GENETICS, 1994, 7 (02) :180-184

[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] Increased amyloid-beta 42(43) in brains of mice expressing mutant presenilin 1 [J].

Duff, K ;

Eckman, C ;

Zehr, C ;

Yu, X ;

Prada, CM ;

Pereztur, J ;

Hutton, M ;

Buee, L ;

Harigaya, Y ;

Yager, D ;

Morgan, D ;

Gordon, MN ;

Holcomb, L ;

Refolo, L ;

Zenk, B ;

Hardy, J ;

Younkin, S .

NATURE, 1996, 383 (6602) :710-713

[9] ALZHEIMER-TYPE NEUROPATHOLOGY IN TRANSGENIC MICE OVEREXPRESSING V717F BETA-AMYLOID PRECURSOR PROTEIN [J].

GAMES, D ;

ADAMS, D ;

ALESSANDRINI, R ;

BARBOUR, R ;

BERTHELETTE, P ;

BLACKWELL, C ;

CARR, T ;

CLEMENS, J ;

DONALDSON, T ;

GILLESPIE, F ;

GUIDO, T ;

HAGOPIAN, S ;

JOHNSONWOOD, K ;

KHAN, K ;

LEE, M ;

LEIBOWITZ, P ;

LIEBERBURG, I ;

LITTLE, S ;

MASLIAH, E ;

MCCONLOGUE, L ;

MONTOYAZAVALA, M ;

MUCKE, L ;

PAGANINI, L ;

PENNIMAN, E ;

POWER, M ;

SCHENK, D ;

SEUBERT, P ;

SNYDER, B ;

SORIANO, F ;

TAN, H ;

VITALE, J ;

WADSWORTH, S ;

WOLOZIN, B ;

ZHAO, J .

NATURE, 1995, 373 (6514) :523-527

[10] Aging renders the brain vulnerable to amyloid β-protein neurotoxicity [J].

Geula, C ;

Wu, CK ;

Saroff, D ;

Lorenzo, A ;

Yuan, ML ;

Yankner, BA .

NATURE MEDICINE, 1998, 4 (07) :827-831

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