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The Human Energy CenterFenton LeBon, MD • nanoNAD+™
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Neuroscience
7 min read•Archived in NAD_Research_Packet.pdf & Dallas2.json

Neurological Resilience: SARM1 Dendritic Pruning & The Adenosine Stress Receptor Axis

How NAD+ metabolism fuels neuronal synaptic plasticity, regulates axonal pruning via SARM1, and modulates adenosine A1/A2A receptors to dampen trauma-induced fear hyperarousal.

“NAD+ infusion offers a mechanistically grounded, physiologically safe route to adenosine receptor activation in PTSD. Unlike direct adenosine administration, NAD+ delivers controlled signaling while supporting neuronal ATP.”

— Dr. Fenton LeBon, MD, MBA

Core Scientific Takeaways

  • Psychological trauma and stress disrupt mitochondrial oxidative phosphorylation in neurons.
  • Extracellular NAD+ is metabolized into adenosine, which activates A1 inhibitory receptors to dampen amygdala hyperarousal.
  • Adenosine A2A receptors activate cAMP-PKA-CREB signaling to support synaptic memory extinction.
  • SARM1 acts to protect neural circuits by cleanly pruning damaged dendrites.

The Energetic Roots of Neuropsychiatric Stress

Under chronic psychological trauma, brain neurons suffer mitochondrial respiration failure. Extracellular NAD+ provides a dual benefit: it fuels neuronal ATP synthesis and is metabolised via ectoenzymes into adenosine. Adenosine acts at A1 receptors to inhibit excessive presynaptic glutamate release in the amygdala, providing physiological calm without addiction.

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