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快速眼动(REM)睡眠行为障碍的发病机制与 REM 睡眠回路的破坏有关。

Breakdown in REM sleep circuitry underlies REM sleep behavior disorder.

机构信息

Systems Neurobiology Laboratory, Departments of Cell and Systems Biology and Physiology, University of Toronto, Ontario, Canada.

Sleep Team, Center of Neuroscience of Lyon, UMR 5292 CNRS/U1028 INSERM, University of Lyon, Lyon, France.

出版信息

Trends Neurosci. 2014 May;37(5):279-88. doi: 10.1016/j.tins.2014.02.009. Epub 2014 Mar 24.

Abstract

During rapid eye movement (REM) sleep, skeletal muscles are almost paralyzed. However, in REM sleep behavior disorder (RBD), which is a rare neurological condition, muscle atonia is lost, leaving afflicted individuals free to enact their dreams. Although this may sound innocuous, it is not, given that patients with RBD often injure themselves or their bed-partner. A major concern in RBD is that it precedes, in 80% of cases, development of synucleinopathies, such as Parkinson's disease (PD). This link suggests that neurodegenerative processes initially target the circuits controlling REM sleep. Clinical and basic neuroscience evidence indicates that RBD results from breakdown of the network underlying REM sleep atonia. This finding is important because it opens new avenues for treating RBD and understanding its link to neurodegenerative disorders.

摘要

在快速眼动 (REM) 睡眠期间,骨骼肌几乎瘫痪。然而,在 REM 睡眠行为障碍 (RBD) 中,这是一种罕见的神经状况,肌肉弛缓会丧失,使受影响的个体可以自由地表现他们的梦境。虽然这听起来无害,但并非如此,因为 RBD 患者经常会伤害自己或他们的床伴。RBD 的一个主要关注点是,在 80%的情况下,它会先于突触核蛋白病(如帕金森病)的发展。这种联系表明,神经退行性过程最初针对控制 REM 睡眠的回路。临床和基础神经科学证据表明,RBD 是 REM 睡眠弛缓的基础网络崩溃的结果。这一发现很重要,因为它为治疗 RBD 开辟了新的途径,并为理解其与神经退行性疾病的联系提供了依据。

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