Resilience in the suprachiasmatic nucleus: Implications for aging and Alzheimer ? s disease

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 di-rections of research that may bridge this conceptual divide and briefly discuss the implications of it for improving health outcomes in later adulthood.

Automated summary

Many believe circadian impairments in aging and Alzheimer's disease are due to tissue degeneration in the central pacemaker, the SCN. However, studies have shown limited atrophy in the SCNs of older individuals and Alzheimer's patients, suggesting the SCN is resilient and not solely responsible for circadian disorganization. Future research directions are proposed to bridge this conceptual gap and improve health outcomes in later adulthood.