Toronto大學(xué)的研究人員首次確定了與帕金森氏癥和其他神經(jīng)退行性疾病密切相關(guān)的嚴(yán)重睡眠障礙的一個(gè)潛在病因。
該研究的主要作者,，John Peever博士說：“我們的研究是第一次建立一個(gè)與人類的REM睡眠行為障礙（RBD）的相關(guān)聯(lián)的可能性,，這很重要，因?yàn)?0%至80%的診斷為RBD的人隨后進(jìn)展為帕金森氏癥或其他神經(jīng)退行性疾病,。”該研究發(fā)表在《The Journal of Neuroscience》上,。
快速動(dòng)眼睡眠行為障礙（RBD）最常見的特征是在做夢(mèng)睡眠（也稱之為快速動(dòng)眼睡眠）中發(fā)生劇烈的運(yùn)動(dòng)?；加蠷BD的人不能體驗(yàn)正常的肌肉松弛,，而這種肌肉松弛可防止他們做夢(mèng)，他們還經(jīng)常由于快速的,、強(qiáng)有力的運(yùn)動(dòng)傷害到自己或傷害到與他們同床的配偶,。在某些情況下，病人需要被固定在床上，以防止嚴(yán)重傷害他們自己或他們同床的配偶,。
Peever的團(tuán)隊(duì)重點(diǎn)研究了RBD的遺傳的原因,，因?yàn)檫@種疾病的根本原因是未知的。有證據(jù)表明,，減少大腦抑制可能會(huì)導(dǎo)致RBD,，所以Peever的團(tuán)隊(duì)利用遺傳性的減少大腦抑制的小鼠，然后記錄他們的睡眠和肌肉活動(dòng),。
Peever說：“我們發(fā)現(xiàn),，減少大腦抑制的小鼠的活動(dòng)就像RBD的患者，而且它們?cè)赗EM睡眠時(shí)會(huì)猛烈的運(yùn)動(dòng),。該聯(lián)系有力地表明,，RBD患者可能有大腦抑制的受損。”
他們還發(fā)現(xiàn),，通過應(yīng)用氯硝西泮可使在小鼠的RBD癥狀緩解,，該藥用于治療人類RBD。
Peever的研究強(qiáng)調(diào)了明確RBD原因的重要性,，因?yàn)?0%至80%的RBD患者在后來會(huì)進(jìn)展為帕金森氏癥,。
Peever說：“治療RBD直接意味著，理解并可能治療帕金森氏病,。”（生物谷Bioon.com）
生物谷推薦原文出處：
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.
