Neural mechanism of age-related decline in circadian rhythmicity

在人类中，衰老与睡眠数量、睡眠质量以及特定的睡眠病理和障碍的变化有关。中枢昼夜节律振荡器功能障碍(SCN，哺乳动物下丘脑视交叉上核)被认为是年龄相关性睡眠障碍的主要原因之一。然而，目前尚不清楚SCN是如何衰老的。在这项研究中，我们通过DNA微阵列的手段，在小鼠的SCN中发现了与年龄相关的分子。在结果中，我们发现了一些在衰老的SCN中表达增加或减少的分子。如果证实这些分子导致SCN功能障碍，它将成为老年人群睡眠障碍的新治疗策略的候选者，并有可能改善老年人的生活质量。

Aging is associated with changes in sleep amount, sleep quality, and specific sleep pathologies and disorders in humans. The dysfunction of the central circadian oscillator (SCN; suprachiasmatic nucleus of the hypothalamus in mammals) is recognized as one of the central causes of age-related sleep disturbances. However, it is still unclear how the SCN become senescent. In this study, we investigated to discover age-related molecules in the mouse SCN by means of DNA microarray. In the result, we found some molecules that the amount of expression increased or decreased in the aged SCN. If it is confirmed that these molecules contribute to the dysfunction of SCN, it would be a candidate for new treatment strategies for sleep disturbances in the aging population and would potentially improve the quality of life for aged individuals.