Breakdown in REM sleep circuitry underlies REM sleep behavior disorder

被引:125
作者
Peever, John [1 ,2 ]
Luppi, Pierre-Herve [3 ]
Montplaisir, Jacques [4 ]
机构
[1] Univ Toronto, Syst Neurobiol Lab, Dept Cell & Syst Biol, Toronto, ON M5S 1A1, Canada
[2] Univ Toronto, Dept Physiol, Toronto, ON M5S 1A1, Canada
[3] Univ Lyon, INSERM, CNRS, Sleep Team,Ctr Neurosci Lyon,UMR 5292,U1028, Lyon, France
[4] Univ Montreal, Hop Sacre Coeur Montreal, Ctr Adv Res Sleep Med, Montreal, PQ, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
EYE-MOVEMENT SLEEP; MILD COGNITIVE IMPAIRMENT; PARKINSONS-DISEASE; BRAIN-STEM; NEURODEGENERATIVE DISEASE; SOMATIC MOTONEURONS; LUMBAR MOTONEURONS; DELAYED EMERGENCE; MUSCLE-ACTIVITY; MOTOR CONTROL;
D O I
10.1016/j.tins.2014.02.009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:279 / 288
页数:10
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