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针对神经胶质细胞阐明亨廷顿病的发病机制。

Targeting glial cells to elucidate the pathogenesis of Huntington's disease.

机构信息

Division of Neuroscience, Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan.

出版信息

Mol Neurobiol. 2010 Jun;41(2-3):248-55. doi: 10.1007/s12035-009-8097-5. Epub 2010 Jan 28.

Abstract

Huntington's disease (HD) is a hereditary neurodegenerative disorder caused by expended CAG repeats in the Huntingtin (Htt) gene. The resultant mutant Htt (mHtt) forms aggregates in neurons and causes neuronal dysfunctions. The major characteristic of HD is the selective loss of neurons in the striatum and cortex, which leads to movement disorders, dementia, and eventual death. Expression of mHtt was also found in non-neuronal cells in the brain, suggesting non-cell-autonomous neurotoxicity in HD. As was documented in many different neurodegenerative disorders, elevated inflammatory responses are also reported in HD. To date, effective treatments for this devastating disease remain to be developed. This review focuses on the importance of glial cells and inflammation in HD pathogenesis. Potential anti-inflammatory interventions for HD are also discussed.

摘要

亨廷顿病(HD)是一种遗传性神经退行性疾病,由亨廷顿(Htt)基因中扩展的 CAG 重复引起。由此产生的突变亨廷顿蛋白(mHtt)在神经元中形成聚集体,导致神经元功能障碍。HD 的主要特征是纹状体和皮层中神经元的选择性丧失,导致运动障碍、痴呆症,最终导致死亡。在大脑中的非神经元细胞中也发现了 mHtt 的表达,这表明 HD 存在非细胞自主的神经毒性。正如在许多不同的神经退行性疾病中所记录的那样,HD 中也报告了炎症反应的升高。迄今为止,这种毁灭性疾病的有效治疗方法仍有待开发。本综述重点介绍了胶质细胞和炎症在 HD 发病机制中的重要性。还讨论了针对 HD 的潜在抗炎干预措施。

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