Neural mechanism of age-related decline in circadian rhythmicity

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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.