Circadian disruption may both precede and worsen major age-related .
Evidence
This review summarizes evidence on Alzheimer's disease, Parkinson's disease, and Huntington's disease, focusing on shared circadian disruptions, oxidative stress, clock gene perturbation, and proposed molecular pathways.
Caveat
The mechanisms linking circadian rhythm disruptions to neurodegeneration remain unclear, limiting therapeutic inference.
Simplified
Disruption of is a recognized hallmark of age-related such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Emerging evidence suggests these disruptions are not merely symptoms but potential causal factors that, in some cases, manifest prior to clinical onset. This points to a bidirectional relationship in which neurodegenerative processes and circadian dysfunction mutually exacerbate each other. Core clock genes, including, and, regulate critical processes such as redox balance, mitochondrial function, and neuroinflammation, which are commonly disrupted in neurodegenerative conditions. Although molecular pathways involving altered protein homeostasis, immune dysregulation, and inflammatory processes are proposed, the precise mechanisms linking circadian rhythm disruptions to neurodegeneration remain unclear. This review provides an integrated overview of shared circadian rhythm disruptions observed in major neurodegenerative diseases and evidence on the underlying molecular mechanisms including oxidative stress and clock gene perturbation, and evaluates the temporal dynamics of circadian disruption relative to disease onset and progression. Furthermore, we discuss the translational potential of circadian-oriented interventions and highlight the limitations of current evidence. Understanding these interactions may help identify novel therapeutic strategies for stabilizing circadian rhythm to mitigate disease progression in neurodegenerative diseases. BMAL1, PER CRY
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