Many believe that the circadian impairments associated with aging and Alzheimer's disease are, simply enough, a byproduct of tissue degeneration within the central pacemaker, the suprachiasmatic nucleus (SCN). However, the findings that have accumulated to date examining the SCNs obtained postmortem from the brains of older individuals, or those diagnosed with Alzheimer's disease upon autopsy, suggest only limited atrophy. We review this literature as well as a complementary one concerning fetal-donor SCN transplant, which established that many circadian timekeeping functions can be maintained with rudimentary (structurally limited) representations of the SCN. Together, these corpora of data suggest that the SCN is a resilient brain region that cannot be directly (or solely) implicated in the behavioral manifestations of circadian disorganization often witnessed during aging as well as early and late progression of Alzheimer's disease. We complete our review by suggesting future directions of research that may bridge this conceptual divide and briefly discuss the implications of it for improving health outcomes in later adulthood.
Keywords: Aging; Alzheimer's disease; Circadian; Neurodegeneration; Phototherapy; Suprachiasmatic nucleus.
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