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亨廷顿病皮质兴奋性过高的发育起源:综述与新观察。

Developmental origins of cortical hyperexcitability in Huntington's disease: Review and new observations.

机构信息

IDDRC, Jane and Terry Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, California.

Section of Neuropathology, Department of Pathology and Laboratory Medicine, University of California Los Angeles, Los Angeles, California.

出版信息

J Neurosci Res. 2019 Dec;97(12):1624-1635. doi: 10.1002/jnr.24503. Epub 2019 Jul 28.

Abstract

Huntington's disease (HD), an inherited neurodegenerative disorder that principally affects striatum and cerebral cortex, is generally thought to have an adult onset. However, a small percentage of cases develop symptoms before 20 years of age. This juvenile variant suggests that brain development may be altered in HD. Indeed, recent evidence supports an important role of normal huntingtin during embryonic brain development and mutations in this protein cause cortical abnormalities. Functional studies also demonstrated that the cerebral cortex becomes hyperexcitable with disease progression. In this review, we examine clinical and experimental evidence that cortical development is altered in HD. We also provide preliminary evidence that cortical pyramidal neurons from R6/2 mice, a model of juvenile HD, are hyperexcitable and display dysmorphic processes as early as postnatal day 7. Further, some symptomatic mice present with anatomical abnormalities reminiscent of human focal cortical dysplasia, which could explain the occurrence of epileptic seizures in this genetic mouse model and in children with juvenile HD. Finally, we discuss recent treatments aimed at correcting abnormal brain development.

摘要

亨廷顿病(HD)是一种遗传性神经退行性疾病,主要影响纹状体和大脑皮层,通常认为其发病年龄在 20 岁以后。然而,有一小部分病例在 20 岁之前出现症状。这种青少年变异表明 HD 可能会改变大脑发育。事实上,最近的证据支持正常亨廷顿蛋白在胚胎大脑发育过程中的重要作用,而该蛋白的突变会导致皮质异常。功能研究还表明,随着疾病的进展,大脑皮层变得过度兴奋。在这篇综述中,我们检查了临床和实验证据,证明 HD 患者的皮质发育发生了改变。我们还提供了初步证据,表明 R6/2 小鼠(一种青少年 HD 模型)的皮质锥体神经元早在出生后 7 天就表现出过度兴奋,并显示出畸形过程。此外,一些出现症状的小鼠表现出类似于人类局灶性皮质发育不良的解剖异常,这可以解释该基因小鼠模型和青少年 HD 儿童中癫痫发作的发生。最后,我们讨论了最近旨在纠正异常大脑发育的治疗方法。

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