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Neuroinflammation is a key component of secondary injury following traumatic brain injury, and anti-inflammatory therapies have been investigated for its regulation (Izzy et al., 2025)

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Advanced insulin resistance, mitochondrial damage from chronic oxidative stress, or inflammatory states can create barriers to AMPK activation and NAD+ utilization that require co-interventions (caloric restriction, anti-inflammatory compounds, or antioxidant support)