The beta A4 amyloid precursor protein gene and Alzheimer's disease

被引:40
作者
Hendriks, L [1 ]
Van Broeckhoven, C [1 ]
机构
[1] UNIV INSTELLING ANTWERP VIB, BORN BUNGE FDN, DEPT BIOCHEM,NEUROGENET LAB, B-2610 ANTWERP, BELGIUM
来源
EUROPEAN JOURNAL OF BIOCHEMISTRY | 1996年 / 237卷 / 01期
关键词
Alzheimer's; proteolysis; beta A4 amyloid precursor protein; beta A4 amyloid; mutation;
D O I
10.1111/j.1432-1033.1996.0006n.x
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 senile dementia caused by progressive neurodegeneration of the central nervous system. One of the most prominent pathological characteristics is beta A4 amyloid deposition in senile plaques in the brain parenchyma and in cerebral blood vessels. beta A4 amyloid is processed from a larger integral membrane protein, the beta A4 amyloid precursor protein. Different pathogenic mutations in this protein have been detected in a small number of Alzheimer's disease families. Here functional implications of these mutations on the processing of the precursor protein and the beta A4 amyloid deposition will be discussed with respect to the pathogenesis of Alzheimer's disease and related disorders.
引用
收藏
页码:6 / 15
页数:10
相关论文
共 123 条
[1]  
[Anonymous], 1907, Centralblatt fur Nervenheilkunde Psychiatrie
[2]   GENERATION OF BETA-AMYLOID IN THE SECRETORY PATHWAY IN NEURONAL AND NONNEURONAL CELLS [J].
BUSCIGLIO, J ;
GABUZDA, DH ;
MATSUDAIRA, P ;
YANKNER, BA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (05) :2092-2096
[3]   RELEASE OF EXCESS AMYLOID BETA-PROTEIN FROM A MUTANT AMYLOID BETA-PROTEIN PRECURSOR [J].
CAI, XD ;
GOLDE, TE ;
YOUNKIN, SG .
SCIENCE, 1993, 259 (5094) :514-516
[4]   APOLIPOPROTEIN-E, EPSILON-4 ALLELE AS A MAJOR RISK FACTOR FOR SPORADIC EARLY AND LATE-ONSET FORMS OF ALZHEIMERS-DISEASE - ANALYSIS OF THE 19Q13.2 CHROMOSOMAL REGION [J].
CHARTIERHARLIN, MC ;
PARFITT, M ;
LEGRAIN, S ;
PEREZTUR, J ;
BROUSSEAU, T ;
EVANS, A ;
BERR, C ;
VIDAL, O ;
ROQUES, P ;
GOURLET, V ;
FRUCHART, JC ;
DELACOURTE, A ;
ROSSOR, M ;
AMOUYEL, P .
HUMAN MOLECULAR GENETICS, 1994, 3 (04) :569-574
[5]   EARLY-ONSET ALZHEIMERS-DISEASE CAUSED BY MUTATIONS AT CODON-717 OF THE BETA-AMYLOID PRECURSOR PROTEIN GENE [J].
CHARTIERHARLIN, MC ;
CRAWFORD, F ;
HOULDEN, H ;
WARREN, A ;
HUGHES, D ;
FIDANI, L ;
GOATE, A ;
ROSSOR, M ;
ROQUES, P ;
HARDY, J ;
MULLAN, M .
NATURE, 1991, 353 (6347) :844-846
[6]  
CHEUNG TT, 1994, INT J EXP CLIN INVES, V1, P30
[7]   EXCESSIVE PRODUCTION OF AMYLOID BETA-PROTEIN BY PERIPHERAL CELLS OF SYMPTOMATIC AND PRESYMPTOMATIC PATIENTS CARRYING THE SWEDISH FAMILIAL ALZHEIMER-DISEASE MUTATION [J].
CITRON, M ;
VIGOPELFREY, C ;
TEPLOW, DB ;
MILLER, C ;
SCHENK, D ;
JOHNSTON, J ;
WINBLAD, B ;
VENIZELOS, N ;
LANNFELT, L ;
SELKOE, DJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (25) :11993-11997
[8]   GENERATION OF AMYLOID-BETA PROTEIN FROM ITS PRECURSOR IS SEQUENCE-SPECIFIC [J].
CITRON, M ;
TEPLOW, DB ;
SELKOE, DJ .
NEURON, 1995, 14 (03) :661-670
[9]   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
[10]   MRC OX-2 ANTIGEN - A LYMPHOID NEURONAL MEMBRANE GLYCOPROTEIN WITH A STRUCTURE LIKE A SINGLE IMMUNOGLOBULIN LIGHT CHAIN [J].
CLARK, MJ ;
GAGNON, J ;
WILLIAMS, AF ;
BARCLAY, AN .
EMBO JOURNAL, 1985, 4 (01) :113-118