Chronic sleep disorders are a major modifiable risk factor for neurodegenerative diseases. However, the mechanisms linking the diverse etiologies of sleep disorders to neuropathology are not fully understood. This review synthesizes evidence to position glymphatic system dysfunction as a critical “mechanistic bridge” linking the multifactorial drivers of disordered sleep, ranging from psychophysiological hyperarousal to intermittent hypoxia and circadian misalignment, to the pathogenesis of neurodegeneration. The brain’s glymphatic system is essential for clearing neurotoxins, such as amyloid-β and α-synuclein, a process that is most efficient during deep, non-rapid eye movement sleep. This review outlines how distinct sleep-disrupting conditions, despite their different origins, converge on a final common pathway: The failure to establish the low-noradrenergic state required for effective glymphatic clearance. This suppression provides a direct mechanism linking poor sleep to the accumulation of toxic proteins that are hallmarks of neurodegenerative diseases. We also explore the evidence for a bidirectional, self-perpetuating cycle, where initial protein accumulation can, in turn, damage sleep-regulating brain nuclei, further degrading sleep and accelerating pathology. This framework reframes the management of all sleep disorders, not merely as symptom control, but as a tangible strategy for neuroprotection.

This study examined how residents of Culiacán, México, adapted over time to prolonged community violence and perceived insecurity. We evaluated a two-speed adaptation theory, which proposes that indicators of acute psychological distress and economic strain decline over time, whereas protective behavioral responses persist as a state of chronic vigilance. A mixed-longitudinal design was employed, consisting of a baseline survey of 1163 residents conducted in October 2024 and a longitudinal cohort of 100 participants followed in February and June 2025. Longitudinal changes were evaluated using Cochran’s Q tests with exact McNemar post hoc comparisons, proportions were reported with 95% Clopper–Pearson confidence intervals, and multivariable logistic regression was used to examine predictors of migration intent. Pharmacologic treatment utilization declined significantly from 36% to 20%, and reported economic strain decreased from 62% to 35% over the study period. In contrast, behavioral routine modifications remained persistently high, decreasing only from 95% to 88%, with no statistically significant longitudinal change. These findings are consistent with the proposed theory, suggesting that while acute psychosocial and economic impacts may diminish over time, protective behavioral adaptations remain comparatively stable. Regarding migration intent, individual economic strain was not significantly associated with the intention to leave the city. Instead, participants who attributed insecurity primarily to social contract collapse, conceptualized as the perceived erosion of community trust, institutional legitimacy, social polarization, and the breakdown of social order, had substantially greater odds of reporting migration intent than those primarily concerned with economic factors (OR = 11.56, 95% CI 1.55–85.98). Overall, these findings suggest that prolonged community violence produces distinct trajectories of psychosocial adaptation, in which acute distress decreases while chronic vigilance persists. Furthermore, migration intentions appear to be more strongly associated with perceived deterioration of the social environment than with individual economic hardship, highlighting the importance of restoring community trust and institutional legitimacy alongside traditional public health and economic interventions.

Glaucoma is conventionally characterized as an intraocular pressure‐dependent optic neuropathy; however, emerging evidence features glaucoma as a complex neurodegenerative disorder of the central nervous system, closely linked to systemic physiological dysregulation. This review aims to combine a rapidly expanding frontier in vision research: the integration of neurotrophic signaling, sleep architecture, and retinal neuroprotection. Neurotrophic factors, particularly the brain‐derived neurotrophic factor‐TrkB axis, are indispensable for the survival and synaptic integrity of retinal ganglion cells. In glaucoma, mechanical and metabolic stressors disrupt the retrograde axonal transport of these survival signals. Furthermore, recent paradigms reveal that neurotrophin expression and downstream signaling cascades are highly modulated by sleep‐wake cycles and circadian rhythms. Sleep fragmentation and chronic sleep disorders, such as obstructive sleep apnea, not only suppress central and ocular neurotrophin synthesis but also exacerbate neuroinflammation, trigger microglial activation, and induce nocturnal ocular perfusion pressure fluctuations. Moreover, the newly characterized ocular glymphatic system shows a highly sleep‐dependent waste clearance mechanism, where sleep deprivation compromises the elimination of neurotoxic aggregates from the optic nerve head. Rather than summarizing this previously separate literature in parallel, this review synthesizes them into a single causal context, explicitly graded by the level of evidentiary certainty, and extends this basis to the clinical dimension of retinal ganglion cell‐related mood disturbance. By integrating these distinct fields, this review proposes an interconnected pathophysiological loop where sleep disturbances diminish neurotrophic support and impair metabolic clearance, rendering retinal ganglion cells highly vulnerable to glaucomatous degeneration. Finally, this review will discuss the therapeutic implications of this network, highlighting chronotherapeutic optimization of intraocular pressure‐lowering agents, small‐molecule TrkB agonists, and targeted sleep interventions as novel, adjuvant neuroprotective strategies. Ultimately, bridging sleep science and sensory neuroscience offers a promising, holistic framework for preserving vision in glaucoma patients.