一项研究发现，老年人常遇到的睡眠混乱——诸如过早睡觉和过早觉醒——可能是由于血液中的激素导致的。Steven A. Brown及其同事比较了来自年轻和年老供体的皮肤细胞的内部生理周期，结果发现这些细胞在牛血清中生长的时候的生物钟是一样的。牛血清是一种营养浆，科研人员通常使用它培养细胞。但是当同样的细胞在来自老年人的人类血清中生长的时候，这种生物钟变得反映出了老年人混乱的睡眠模式。此前的研究已经证明了人的睡眠-觉醒周期随着衰老而变得越来越提前，这可能导致断断续续的和休息得不好的睡眠，以及更频繁的日间打盹。一些科研人员已经提出了一些理论——日光的减少或更少户外活动——从而解释这种与年龄有关的现象。然而，当前这项研究提示，血清中的一种激素或其中的其它循环因素改变了正在衰老的细胞的生物钟。这组作者说，如果与年龄有关的睡眠混乱确实源于激素的作用，那么就有可能用药物加以治疗。（生物谷Bioon.com）
生物谷推荐原文出处：
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.
