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In particular, they found that, in the absence of BMAL1, NF-κB-driven transcription was upregulated by the core circadian protein CLOCK, whereas BMAL1 hindered the CLOCK-induced increase in the activation of NF-κB-regulated genes 71

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The convergence of synaptic dysfunction, mitochondrial failure, neuroinflammation, and impaired protein clearance underscores the complexity of the disease and the need for early, multi-mechanistic neuroprotective interventions