β-peptide immunization -: A possible new treatment for Alzheimer disease

被引：68

作者：

Schenk, DB ^{[1
]}

Seubert, P ^{[1
]}

Lieberburg, I ^{[1
]}

Wallace, J ^{[1
]}

机构：

[1] Elan Pharmaceut, S San Francisco, CA 94080 USA

来源：

ARCHIVES OF NEUROLOGY | 2000年 / 57卷 / 07期

关键词：

D O I：

10.1001/archneur.57.7.934

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Research on the pathophysiological characteristics of Alzheimer disease (AD) over the past decade has been directed toward the ultimate goal of developing a disease-modifying treatment to control or prevent the disease. A report recently published in Nature(1) describes for the first time a treatment that may both prevent and treat the progression of Alzheimer disease. The treatment ironically involves immunization with the pathological p-amyloid peptide itself to generate an immune response targeted against the amyloid plaques in the brain. These findings have raised a number of scientific and clinical questions that are discussed below.

引用

页码：934 / 936

页数：3

共 23 条

[1] Neuropsychological function and Apolipoprotein E genotype in the preclinical detection of Alzheimer's disease [J].

Bondi, MW ;

Salmon, DP ;

Galasko, D ;

Thomas, RG ;

Thal, LJ .

PSYCHOLOGY AND AGING, 1999, 14 (02) :295-303

[2] 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

[3] Transcytosis of protein through the mammalian cerebral epithelium and endothelium .3. Receptor-mediated transcytosis through the blood-brain barrier of blood-borne transferrin and antibody against the transferrin receptor [J].

Broadwell, RD ;

BakerCairns, BJ ;

Friden, PM ;

Oliver, C ;

Villegas, JC .

EXPERIMENTAL NEUROLOGY, 1996, 142 (01) :47-65

[4] SERUM-PROTEINS BYPASS THE BLOOD-BRAIN FLUID BARRIERS FOR EXTRACELLULAR ENTRY TO THE CENTRAL-NERVOUS-SYSTEM [J].

BROADWELL, RD ;

SOFRONIEW, MV .

EXPERIMENTAL NEUROLOGY, 1993, 120 (02) :245-263

[5] 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

[6] MUTATION OF THE BETA-AMYLOID PRECURSOR PROTEIN IN FAMILIAL ALZHEIMERS-DISEASE INCREASES BETA-PROTEIN PRODUCTION [J].

CITRON, M ;

OLTERSDORF, T ;

HAASS, C ;

MCCONLOGUE, L ;

HUNG, AY ;

SEUBERT, P ;

VIGOPELFREY, C ;

LIEBERBURG, I ;

SELKOE, DJ .

NATURE, 1992, 360 (6405) :672-674

[7] 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

[8] INHIBITION OF BETA-AMYLOID FORMATION IDENTIFIES PROTEOLYTIC PRECURSORS AND SUBCELLULAR SITE OF CATABOLISM [J].

HIGAKI, J ;

QUON, D ;

ZHONG, ZY ;

CORDELL, B .

NEURON, 1995, 14 (03) :651-659

[9] Correlative memory deficits, A beta elevation, and amyloid plaques in transgenic mice [J].

Hsiao, K ;

Chapman, P ;

Nilsen, S ;

Eckman, C ;

Harigaya, Y ;

Younkin, S ;

Yang, FS ;

Cole, G .

SCIENCE, 1996, 274 (5284) :99-102

[10] Altered metabolism of familial Alzheimer's disease-linked amyloid precursor protein variants in yeast artificial chromosome transgenic mice [J].

Lamb, BT ;

Call, LM ;

Slunt, HH ;

Bardel, KA ;

Lawler, AM ;

Eckman, CB ;

Younkin, SG ;

Holtz, G ;

Wagner, SL ;

Price, DL ;

Sisodia, SS ;

Gearhart, JD .

HUMAN MOLECULAR GENETICS, 1997, 6 (09) :1535-1541

← 1 2 3 →