Telomere shortening in neurological disorders: an abundance of unanswered questions.

Telomere shortening in neurological disorders: an abundance of unanswered questions.
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DOI:
10.1016/j.tins.2014.02.010
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发表时间:
2014-05
影响因子:
15.9
通讯作者:
Mattson MP
Mattson MP
中科院分区:
医学1区
文献类型:
--
作者:
Eitan E;Hutchison ER;Mattson MP

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端粒,核糖核蛋白复合物的帽子真核生物染色体,通常缩短白细胞老化。衰老是神经退行性疾病(ND)的主要危险因素,并且已经出现了一种常见的假设,即白细胞端粒长度(LTL)可以作为神经系统疾病的预测因子。然而,阿尔茨海默病和帕金森病患者LTL较短的证据并不一致。端粒缩短的不同原因可以解释研究和个体之间LTL的差异。需要进一步的研究来确定神经元和神经胶质细胞端粒是否在衰老和神经退行性疾病中缩短,LTL是否以及如何与脑细胞端粒缩短相关,以及端粒缩短是否在神经系统疾病中起因果作用或加剧神经系统疾病。
Telomeres, ribonucleoprotein complexes that cap eukaryotic chromosomes, typically shorten in leukocytes with aging. Aging is a primary risk factor for neurodegenerative disease (ND), and a common assumption has arisen that leukocyte telomere length (LTL) can serve as a predictor of neurological disease. However, the evidence for shorter LTL in Alzheimer’s and Parkinson’s patients is inconsistent. The diverse causes of telomere shortening may explain variability in LTL between studies and individuals. Additional research is needed to determine whether neuronal and glial telomeres shorten during aging and in neurodegenerative disorders, if and how LTL is related to brain cell telomere shortening, and whether telomere shortening plays a causal role in or exacerbates neurological disorders.
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