Substantial progress has been made toward understanding the neuropathology, genetic origins, and epidemiology of neurodegenerative diseases, including Alzheimer's disease; tauopathies, such as frontotemporal dementia; α-synucleinopathies, such as Parkinson's disease or dementia with Lewy bodies; Huntington's disease; and amyotrophic lateral sclerosis with dementia, as well as prion diseases. Recent evidence has implicated dendritic spine dysfunction as an important substrate of the pathogenesis of dementia in these disorders. Dendritic spines are specialized structures, extending from the neuronal processes, on which excitatory synaptic contacts are formed, and the loss of dendritic spines correlates with the loss of synaptic function. We review the literature that has implicated direct or indirect structural alterations at dendritic spines in the pathogenesis of major neurodegenerative diseases, focusing on those that lead to dementias such as Alzheimer's, Parkinson's, and Huntington's diseases, as well as frontotemporal dementia and prion diseases. We stress the importance of in vivo studies in animal models.

中文翻译：

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神经退行性疾病中的树突棘病理学。

在了解神经退行性疾病（包括阿尔茨海默氏病）的神经病理学，遗传起源和流行病学方面已经取得了实质性进展。taopathies，例如额颞痴呆；α-突触核蛋白病，如帕金森氏病或路易体痴呆；亨廷顿氏病; 以及患有痴呆的肌萎缩性侧索硬化症和病毒疾病。最近的证据表明，树突状脊柱功能障碍是这些疾病中痴呆症发病机理的重要底物。树突棘是从神经元过程延伸的特殊结构，在其上形成兴奋性突触接触，并且树突棘的丧失与突触功能的丧失相关。我们回顾了在主要神经退行性疾病的发病机理中涉及树突棘直接或间接结构改变的文献，重点是那些导致痴呆症的疾病，例如阿尔茨海默氏症，帕金森氏症和亨廷顿氏症以及额颞叶痴呆和病毒病。我们强调在动物模型中进行体内研究的重要性。