The cerebellum in Alzheimer's disease: evaluating its role in cognitive decline

The cerebellum in Alzheimer's disease: evaluating its role in cognitive decline
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DOI:
10.1093/brain/awx194
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发表时间:
2018-01-01
期刊:
影响因子:
14.5
通讯作者:
Schmahmann, Jeremy D.
Schmahmann, Jeremy D.
中科院分区:
医学1区
文献类型:
--
作者:
Jacobs, Heidi I. L.;Hopkins, David A.;Schmahmann, Jeremy D.

文献摘要

被引文献

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小脑长期以来被认为是协调自主运动活动和运动学习所必需的。解剖学,临床和神经影像学研究已经导致了对小脑在神经系统功能中作用的理解的范式转变,表明小脑似乎也是认知和情感调节的组成部分。研究小脑对认知过程的贡献增加了人们对探索小脑在神经退行性疾病和神经精神疾病中的作用的兴趣。其中最主要的是老年痴呆症。在这里,我们回顾了一个已经相当大的现有文献的神经病理学,结构和功能的神经影像学研究小脑在阿尔茨海默氏病。我们认为这些观察结果的特点阿尔茨海默氏病的认知功能障碍,并在这样做,我们介绍了一个新的视角,其病理生理学和表现。我们提出了一个综合性的假设,有一个小脑的贡献,在阿尔茨海默氏症的认知和神经精神缺陷。我们借鉴了辨距障碍的思想理论,表明这小脑组件表现为赤字调制的神经行为缺陷。我们为未来的研究提供了建议,以调查这一假设,并最终建立一个全面的,因果的临床病理疾病模型。
The cerebellum has long been regarded as essential only for the coordination of voluntary motor activity and motor learning. Anatomical, clinical and neuroimaging studies have led to a paradigm shift in the understanding of the cerebellar role in nervous system function, demonstrating that the cerebellum appears integral also to the modulation of cognition and emotion. The search to understand the cerebellar contribution to cognitive processing has increased interest in exploring the role of the cerebellum in neurodegenerative and neuropsychiatric disorders. Principal among these is Alzheimer's disease. Here we review an already sizeable existing literature on the neuropathological, structural and functional neuroimaging studies of the cerebellum in Alzheimer's disease. We consider these observations in the light of the cognitive deficits that characterize Alzheimer's disease and in so doing we introduce a new perspective on its pathophysiology and manifestations. We propose an integrative hypothesis that there is a cerebellar contribution to the cognitive and neuropsychiatric deficits in Alzheimer's disease. We draw on the dysmetria of thought theory to suggest that this cerebellar component manifests as deficits in modulation of the neurobehavioural deficits. We provide suggestions for future studies to investigate this hypothesis and, ultimately, to establish a comprehensive, causal clinicopathological disease model.