Researchers at Ottawa Hospital Research Institute and University of Ottawa found that high risk of obstructive sleep apnea was associated with approximately 40% higher odds of a composite poor mental health outcome at baseline and follow-up among adults aged 45–85 years in the Canadian Longitudinal Study on Aging.

Identifying factors associated with mental health outcomes is an important goal on several fronts. Mental health conditions rank among the leading contributors to global disease burden, with anxiety and depressive disorders described as most common. Individuals living with mental health conditions face higher risks of cardiometabolic diseases, unemployment, homelessness, disability, and hospitalizations. Economically, mental disorders carry an estimated $1 trillion annual global cost in lost productivity.

Obstructive sleep apnea (OSA) involves repeated upper airway narrowing during sleep. Disturbed breathing can break up sleep (sleep fragmentation), trigger a stress response in the nervous system (sympathetic activation), and cause episodes of low oxygen in the blood (intermittent hypoxemia).

Using this method showed “the largest improvement in memory” anyone has ever found, according to one expert.

Lipofuscin, a marker of aging, is the accumulation of autofluorescent granules within microglia and postmitotic cells such as neurons. Lipofuscin has traditionally been regarded as an inert byproduct of cellular degradation. However, recent findings suggest that lipofuscin may play a role in modulating age-related neurodegenerative processes, and several questions remain unanswered. For instance, why do lipofuscin granules accumulate preferentially in aged neurons and microglia? What happens to these pigments upon neuronal demise? Particularly in neurodegenerative diseases like Alzheimer’s disease (AD), why does amyloid β (Aβ) deposition usually begin in late adulthood or during aging? Why do lipofuscin and amyloid plaques appear preferentially in grey matter and rarely in white matter? In this review, we argue that lipofuscin should be revisited not as a simple biomarker of aging, but as a potential modulator of neurodegenerative diseases. We synthesize emerging evidence linking lipofuscin to lysosomal dysfunction, oxidative stress, lipid peroxidation and disease onset—mechanisms critically implicated in neurodegeneration. We also explore the potential interactions of lipofuscin with Aβ and their spatial location, and summarize evidence showing that lipofuscin may influence disease progression via feedback loops affecting cellular clearance and inflammation. Finally, we propose future research directions toward better understanding of the mechanisms of lipofuscin accumulation and improved lysosomal waste clearance in aging.