Tropospheric ozone, a highly reactive air pollutant, has emerged as a potential environmental risk factor for Alzheimer's disease (AD) and its associated sleep disturbances, yet a comprehensive synthesis of the underlying mechanisms has remained limited. This narrative review summarizes experimental and epidemiological evidence on ozone exposure, neurodegeneration and disrupted sleep, organized around one working hypothesis: ozone generates a systemic oxidative-inflammatory signal that reaches the central nervous system, with sleep/circadian disruption and AD-related pathology as downstream outcomes that may reinforce each other. In experimental models, ozone is associated with oxidative stress, mitochondrial dysfunction, blood-brain barrier disruption, glial activation and neuroinflammation, overlapping with β-amyloid accumulation and tau hyperphosphorylation, and with reduced REM sleep and altered neurotransmitters; clock-gene changes have been shown mainly in peripheral tissue. Circadian disruption is a candidate effector, and current data cannot distinguish mediation from co-occurrence. Epidemiological evidence for ozone-specific associations with cognitive decline remains inconsistent at the population level compared with other pollutants such as PM2.5 or NO2, although some cohorts report pollutant-specific effects and modulation by the apolipoprotein E ε4 (APOE4) genotype. Most experimental studies use concentrations well above regulatory ambient standards. Overall, ambient ozone is a biologically plausible, but not yet epidemiologically confirmed, candidate risk factor for AD and sleep disorders. Future work should prioritize exposure-graded longitudinal studies and clarification of the dose-response relationship, including the effects of controlled medical ozone.
