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What Happens with the Circuit in Alzheimer's Disease in Mice and Humans?
Annual Review of Neuroscience ( IF 12.1 ) Pub Date : 2018-07-09 00:00:00 , DOI: 10.1146/annurev-neuro-080317-061725
Benedikt Zott 1, 2, 3 , Marc Aurel Busche 4, 5 , Reisa A Sperling 5, 6, 7 , Arthur Konnerth 1, 2, 3
Affiliation  

A major mystery of many types of neurological and psychiatric disorders, such as Alzheimer's disease (AD), remains the underlying, disease-specific neuronal damage. Because of the strong interconnectivity of neurons in the brain, neuronal dysfunction necessarily disrupts neuronal circuits. In this article, we review evidence for the disruption of large-scale networks from imaging studies of humans and relate it to studies of cellular dysfunction in mouse models of AD. The emerging picture is that some forms of early network dysfunctions can be explained by excessively increased levels of neuronal activity. The notion of such neuronal hyperactivity receives strong support from in vivo and in vitro cellular imaging and electrophysiological recordings in the mouse, which provide mechanistic insights underlying the change in neuronal excitability. Overall, some key aspects of AD-related neuronal dysfunctions in humans and mice are strikingly similar and support the continuation of such a translational strategy.

中文翻译:


小鼠和人类阿尔茨海默氏病的回路发生了什么?

许多类型的神经和精神疾病(例如阿尔茨海默氏病(AD))的主要谜团仍然是潜在的,特定于疾病的神经元损害。由于大脑中神经元的强互连性,神经元功能障碍必然会破坏神经元回路。在本文中,我们将从人类的影像学研究中回顾大规模网络破坏的证据,并将其与AD小鼠模型中细胞功能障碍的研究联系起来。新兴的现象是,某些形式的早期网络功能障碍可以通过神经元活动水平的过度增加来解释。这种神经元活动亢进的概念得到了小鼠体内和体外细胞成像和电生理记录的有力支持,这为潜在的神经元兴奋性变化提供了机械学见解。

更新日期:2018-07-09
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