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阿尔茨海默病的异质性:来自细胞放射敏感性及该表型互补性的证据。

Heterogeneity in Alzheimer's disease: evidence from cellular radiosensitivity and complementation of this phenotype.

作者信息

Chen P, Kidson C, Lavin M

机构信息

Queensland Institute of Medical Research, Brisbane, Australia.

出版信息

Mutat Res. 1991 Jan;256(1):21-7. doi: 10.1016/0921-8734(91)90029-b.

Abstract

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.

摘要

通过检测淋巴母细胞系中的克隆形成存活率和辐射诱导的染色体畸变,对一系列阿尔茨海默病(AD)患者和正常对照的辐射敏感性进行了研究。AD患者和正常人在暴露于γ射线后基于集落存活的D0值分别为0.86±0.04和1.14±0.03 Gy。然而,2个AD细胞系的D0值在正常范围内。这些AD细胞中辐射敏感性的增加通过这些细胞中γ射线诱导的染色体畸变数量的增加得到证实。采用细胞融合技术,以辐射诱导的染色体畸变频率作为区分不同组别的手段,研究AD中辐射敏感表型不同互补组的存在情况。在5个AD细胞系中发现了4个互补组。这些发现为AD的异质性提供了额外的实验证据。

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