一項(xiàng)研究發(fā)現(xiàn)，老年人常遇到的睡眠混亂——諸如過早睡覺和過早覺醒——可能是由于血液中的激素導(dǎo)致的,。Steven A. Brown及其同事比較了來自年輕和年老供體的皮膚細(xì)胞的內(nèi)部生理周期,，結(jié)果發(fā)現(xiàn)這些細(xì)胞在牛血清中生長(zhǎng)的時(shí)候的生物鐘是一樣的。牛血清是一種營(yíng)養(yǎng)漿,，科研人員通常使用它培養(yǎng)細(xì)胞,。但是當(dāng)同樣的細(xì)胞在來自老年人的人類血清中生長(zhǎng)的時(shí)候，這種生物鐘變得反映出了老年人混亂的睡眠模式,。此前的研究已經(jīng)證明了人的睡眠-覺醒周期隨著衰老而變得越來越提前,，這可能導(dǎo)致斷斷續(xù)續(xù)的和休息得不好的睡眠，以及更頻繁的日間打盹,。一些科研人員已經(jīng)提出了一些理論——日光的減少或更少戶外活動(dòng)——從而解釋這種與年齡有關(guān)的現(xiàn)象,。然而，當(dāng)前這項(xiàng)研究提示,，血清中的一種激素或其中的其它循環(huán)因素改變了正在衰老的細(xì)胞的生物鐘,。這組作者說，如果與年齡有關(guān)的睡眠混亂確實(shí)源于激素的作用,，那么就有可能用藥物加以治療,。（生物谷Bioon.com）
生物谷推薦原文出處：
PNAS doi: 10.1073/pnas.1008882108
Serum factors in older individuals change cellular clock properties
Lucia Pagania,b, Karen Schmitta, Fides Meiera, Jan Izakovicc, Konstanze Roemerd, Antoine Violae, Christian Cajochene, Anna Wirz-Justicee, Steven A. Brownb,1,2, and Anne Eckerta,1,2
Abstract
Human aging is accompanied by dramatic changes in daily sleep–wake behavior: Activity shifts to an earlier phase, and the consolidation of sleep and wake is disturbed. Although this daily circadian rhythm is brain-controlled, its mechanism is encoded by cell-autonomous circadian clocks functioning in nearly every cell of the body. In fact, human clock properties measured in peripheral cells such as fibroblasts closely mimic those measured physiologically and behaviorally in the same subjects. To understand better the molecular mechanisms by which human aging affects circadian clocks, we characterized the clock properties of fibroblasts cultivated from dermal biopsies of young and older subjects. Fibroblast period length, amplitude, and phase were identical in the two groups even though behavior was not, thereby suggesting that basic clock properties of peripheral cells do not change during aging. Interestingly, measurement of the same cells in the presence of human serum from older donors shortened period length and advanced the phase of cellular circadian rhythms compared with treatment with serum from young subjects, indicating that a circulating factor might alter human chronotype. Further experiments demonstrated that this effect is caused by a thermolabile factor present in serum of older individuals. Thus, even though the molecular machinery of peripheral circadian clocks does not change with age, some age-related circadian dysfunction observed in vivo might be of hormonal origin and therefore might be pharmacologically remediable.
