Toronto大学的研究人员首次确定了与帕金森氏症和其他神经退行性疾病密切相关的严重睡眠障碍的一个潜在病因。
该研究的主要作者，John Peever博士说：“我们的研究是第一次建立一个与人类的REM睡眠行为障碍（RBD）的相关联的可能性，这很重要，因为60%至80%的诊断为RBD的人随后进展为帕金森氏症或其他神经退行性疾病。”该研究发表在《The Journal of Neuroscience》上。
快速动眼睡眠行为障碍（RBD）最常见的特征是在做梦睡眠（也称之为快速动眼睡眠）中发生剧烈的运动。患有RBD的人不能体验正常的肌肉松弛，而这种肌肉松弛可防止他们做梦，他们还经常由于快速的、强有力的运动伤害到自己或伤害到与他们同床的配偶。在某些情况下，病人需要被固定在床上，以防止严重伤害他们自己或他们同床的配偶。
Peever的团队重点研究了RBD的遗传的原因，因为这种疾病的根本原因是未知的。有证据表明，减少大脑抑制可能会导致RBD，所以Peever的团队利用遗传性的减少大脑抑制的小鼠，然后记录他们的睡眠和肌肉活动。
Peever说：“我们发现，减少大脑抑制的小鼠的活动就像RBD的患者，而且它们在REM睡眠时会猛烈的运动。该联系有力地表明，RBD患者可能有大脑抑制的受损。”
他们还发现，通过应用氯硝西泮可使在小鼠的RBD症状缓解，该药用于治疗人类RBD。
Peever的研究强调了明确RBD原因的重要性，因为60%至80%的RBD患者在后来会进展为帕金森氏症。
Peever说：“治疗RBD直接意味着，理解并可能治疗帕金森氏病。”（生物谷Bioon.com）
生物谷推荐原文出处：
The Journal of Neuroscience DOI: 10.1523/?JNEUROSCI.0347-11.2011
Impaired GABA and Glycine Transmission Triggers Cardinal Features of Rapid Eye Movement Sleep Behavior Disorder in Mice
Patricia L. Brooks and John H. Peever
Rapid eye movement (REM) sleep behavior disorder (RBD) is a neurological disease characterized by loss of normal REM motor inhibition and subsequent dream enactment. RBD is clinically relevant because it predicts neurodegenerative disease onset (e.g., Parkinson's disease) and is clinically problematic because it disrupts sleep and results in patient injuries and hospitalization. Even though the cause of RBD is unknown, multiple lines of evidence indicate that abnormal inhibitory transmission underlies the disorder. Here, we show that transgenic mice with deficient glycine and GABA transmission have a behavioral, motor, and sleep phenotype that recapitulates the cardinal features of RBD. Specifically, we show that mice with impaired glycine and GABAA receptor function exhibit REM motor behaviors, non-REM muscle twitches, sleep disruption, and EEG slowing—the defining disease features. Importantly, the RBD phenotype is rescued by drugs (e.g., clonazepam and melatonin) that are routinely used to treat human disease symptoms. Our findings are the first to identify a potential mechanism for RBD—we show that deficits in glycine- and GABAA-mediated inhibition trigger the full spectrum of RBD symptoms. We propose that these mice are a useful resource for investigating in vivo disease mechanisms and developing potential therapeutics for RBD.
