神经退行性疾病的端粒长度减少可能提示共享生物学。

Lakshmi Narayanan Kota, Srikala Bharath, Meera Purushottam, Nagaraj S Moily, Palanimuthu Thangaraju Sivakumar, Mathew Varghese, Pramod Kumar Pal, Sanjeev Jain
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引用次数: 36

摘要

细胞早期死亡是神经退行性疾病的一个特征。端粒缩短与细胞过早衰老有关,可能是神经系统疾病细胞病理的标志。以相对端粒拷贝/单拷贝基因比率测量痴呆(N=70)、亨廷顿病(N=35)、失调性毛细血管扩张症(N=9)和年龄组匹配对照样本(N=105)的相对端粒长度。亨廷顿氏病患者端粒拷贝/单拷贝基因相对比值最低(0.21),其次是共济失调毛细血管扩张(0.31)和痴呆(0.48)。年轻对照组的相对端粒拷贝/单拷贝基因比最高(1.07)。端粒长度的减少可能表明,这些疾病共同的生物学途径有助于细胞衰老。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reduced telomere length in neurodegenerative disorders may suggest shared biology.

Early cell death is a feature of neurodegenerative disorders. Telomere shortening is related to premature cellular senescence and could be a marker for cellular pathology in neurological diseases. Relative telomere length in dementia (N=70), Huntington's disease (N=35), ataxia telangiectasia (N=9), and age-group matched control samples (N=105) was measured as relative telomere copy/single copy gene ratios. Individuals with Huntington's disease had the lowest relative telomere copy/single copy gene ratio (0.21), followed by ataxia telangiectasia (0.31) and dementia (0.48). The younger control group had the highest relative telomere copy/single copy gene ratio (1.07). The reduced telomere length could be indicative of shared biological pathways across these disorders contributing to cellular senescence.

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