HETEROGENEITY IN ALZHEIMERS-DISEASE - EVIDENCE FROM CELLULAR RADIOSENSITIVITY AND COMPLEMENTATION OF THIS PHENOTYPE

被引:8
作者
CHEN, P
KIDSON, C
LAVIN, M
机构
[1] Queensland Institute of Medical Research, Brisbane
来源
MUTATION RESEARCH | 1991年 / 256卷 / 01期
基金
英国医学研究理事会;
关键词
RADIOSENSITIVITY; ALZHEIMERS DISEASE; LYMPHOBLASTOID CELLS; COMPLEMENTATION; HETEROGENEITY; CHROMOSOME ABERRATIONS;
D O I
10.1016/0921-8734(91)90029-B
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Radiosensitivity was studied in a series of Alzheimer's disease (AD) patients and normal controls by examining clonogenic survival and radiation-induced chromosome aberrations in lymphoblastoid cell lines. D0 values based on colony survival for AD and normals following exposure to gamma-rays were 0.86 +/- 0.04 and 1.14 +/- 0.03 Gy respectively. However, 2 of the AD cell lines had D0 values in the normal range. This increased radiosensitivity in AD cells was confirmed by an increased number of gamma-ray-induced chromosome aberrations in these cells. Cell fusion was employed to investigate the presence of different complementation groups for the radiosensitive phenotype in AD using frequency of radiation-induced chromosome aberrations as a means of distinguishing different groups. Four complementation groups were found among 5 AD cell lines. These findings provide additional experimental evidence in support of heterogeneity in AD.
引用
收藏
页码:21 / 27
页数:7
相关论文
共 39 条
  • [1] COMPARISON OF GAMMA-RADIATION-INDUCED ACCUMULATION OF ATAXIA TELANGIECTASIA AND CONTROL-CELLS IN G2 PHASE
    BATES, PR
    LAVIN, MF
    [J]. MUTATION RESEARCH, 1989, 218 (02): : 165 - 170
  • [2] BERGENER M, 1972, ACTA GERONTOL, V2, P359
  • [3] PHENOTYPIC HETEROGENEITY IN FAMILIAL ALZHEIMERS-DISEASE - A STUDY OF 24 KINDREDS
    BIRD, TD
    SUMI, SM
    NEMENS, EJ
    NOCHLIN, D
    SCHELLENBERG, G
    LAMPE, TH
    SADOVNICK, A
    CHUI, H
    MINER, GW
    TINKLENBERG, J
    [J]. ANNALS OF NEUROLOGY, 1989, 25 (01) : 12 - 25
  • [4] ALZHEIMERS-DISEASE - CHOLINE-ACETYLTRANSFERASE ACTIVITY IN BRAIN-TISSUE FROM CLINICAL AND PATHOLOGICAL SUBGROUPS
    BIRD, TD
    STRANAHAN, S
    SUMI, SM
    RASKIND, M
    [J]. ANNALS OF NEUROLOGY, 1983, 14 (03) : 284 - 293
  • [5] CHROMOSOME CHANGES IN ALZHEIMERS PRESENILE-DEMENTIA
    BUCKTON, KE
    WHALLEY, LJ
    LEE, M
    CHRISTIE, JE
    [J]. JOURNAL OF MEDICAL GENETICS, 1983, 20 (01) : 46 - 51
  • [6] GENE DOSAGE AND COMPLEMENTATION ANALYSIS OF ATAXIA TELANGIECTASIA LYMPHOBLASTOID CELL-LINES ASSAYED BY INDUCED CHROMOSOME-ABERRATIONS
    CHEN, P
    IMRAY, FP
    KIDSON, C
    [J]. MUTATION RESEARCH, 1984, 129 (02): : 165 - 172
  • [7] IDENTIFICATION OF ATAXIA TELANGIECTASIA HETEROZYGOTES, A CANCER PRONE POPULATION
    CHEN, PC
    LAVIN, MF
    KIDSON, C
    MOSS, D
    [J]. NATURE, 1978, 274 (5670) : 484 - 486
  • [8] CLINICAL SUBTYPES OF DEMENTIA OF THE ALZHEIMER TYPE
    CHUI, HC
    TENG, EL
    HENDERSON, VW
    MOY, AC
    [J]. NEUROLOGY, 1985, 35 (11) : 1544 - 1550
  • [9] ALZHEIMERS-DISEASE - A DISORDER OF CORTICAL CHOLINERGIC INNERVATION
    COYLE, JT
    PRICE, DL
    DELONG, MR
    [J]. SCIENCE, 1983, 219 (4589) : 1184 - 1190
  • [10] SYMPTOMS OF X-RAY DAMAGE TO RADIOSENSITIVE MOUSE LEUKEMIC-CELLS - ASYNCHRONOUS POPULATIONS
    EHMANN, UK
    NAGASAWA, H
    PETERSEN, DF
    LETT, JT
    [J]. RADIATION RESEARCH, 1974, 60 (03) : 453 - 472