Age-dependent association between butyrylcholinesterase K-variant and Alzheimer disease-related neuropathology in human brains

被引:19
作者
Ghebremedhin, E
Thal, DR
Schultz, C
Braak, H
机构
[1] Univ Frankfurt, Dept Clin Neuroanat, D-60590 Frankfurt, Germany
[2] Univ Bonn, Med Ctr, Inst Neuropathol, D-53105 Bonn, Germany
关键词
Alzheimer disease; Alzheimer disease neuropathology; butyrylcholinesterase; K-variant; apolipoprotein E; genetic association;
D O I
10.1016/S0304-3940(02)00014-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The association between the K-variant of the butyrylcholinesterase gene (BCHE-K) and Alzheimer disease (AD) or AD-related neuropathology has been reported to date with conflicting results. Here, we determined in a sample of 521 cases the severity of AD-related neuropathology and the polymorphisms of both BCHE-K and apolipoprotein E (ApoE). Histopathologically, all brains were classified according to procedures permitting differentiation of the evolutionary stages of neurofibrillary tangles (NFTs) and amyloid-beta-protein deposition (Abeta-deposits). The results show that the association between BCHE-K and AD-related neuropathology only was limited to homozygotes for the K allele (P = 0.036 for NFTs, and P = 0.045 for Abeta-deposits) at ages greater than or equal to70years but not 50-69 years. Furthermore, no interaction was apparent between BCHE-K and ApoE. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:25 / 28
页数:4
相关论文
共 20 条
[1]  
BARTELS CF, 1992, AM J HUM GENET, V50, P1086
[2]   Frequency of stages of Alzheimer-related lesions in different age categories [J].
Braak, H ;
Braak, E .
NEUROBIOLOGY OF AGING, 1997, 18 (04) :351-357
[3]   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
[4]   The butyrylcholinesterase gene is neither independently nor synergistically associated with late-onset AD in clinic- and community-based populations [J].
Crawford, F ;
Fallin, D ;
Suo, Z ;
Abdullah, L ;
Gold, M ;
Gauntlett, A ;
Duara, R ;
Mullan, M .
NEUROSCIENCE LETTERS, 1998, 249 (2-3) :115-118
[5]   Improved method facilitates reliable APOE genotyping of genomic DNA extracted from formaldehyde-fixed pathology specimens [J].
Ghebremedhin, E ;
Braak, H ;
Braak, E ;
Sahm, J .
JOURNAL OF NEUROSCIENCE METHODS, 1998, 79 (02) :229-231
[6]   High frequency of apolipoprotein E ε4 allele in young individuals with very mild Alzheimer's disease-related neurofibrillary changes [J].
Ghebremedhin, E ;
Schultz, C ;
Braak, E ;
Braak, H .
EXPERIMENTAL NEUROLOGY, 1998, 153 (01) :152-155
[7]   Gender and age modify the association between APOE and AD-related neuropathology [J].
Ghebremedhin, E ;
Schultz, C ;
Thal, DR ;
Rüb, U ;
Ohm, TG ;
Braak, E ;
Braak, H .
NEUROLOGY, 2001, 56 (12) :1696-1701
[8]   Analysis of association between Alzheimer disease and the K variant of butyrylcholinesterase (BCHE-K) [J].
Grubber, JM ;
Saunders, AM ;
Crane-Gatherum, AR ;
Scott, WK ;
Martin, ER ;
Haynes, CS ;
Conneally, PM ;
Small, GW ;
Roses, AD ;
Haines, JL ;
Pericak-Vance, MA .
NEUROSCIENCE LETTERS, 1999, 269 (02) :115-119
[9]   Editorial on consensus recommendations for the postmortem diagnosis of Alzheimer disease from the National Institute on Aging and the Reagan Institute working group on diagnostic criteria for the neuropathological assessment of Alzheimer disease [J].
Hyman, BT ;
Trojanowski, JQ .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1997, 56 (10) :1095-1097
[10]   Detection of the plasma cholinesterase K variant by PCR using an amplification-created restriction site [J].
Jensen, FS ;
Nielsen, LR ;
Schwartz, M .
HUMAN HEREDITY, 1996, 46 (01) :26-31