
AMPAR Up-Regulation & Neuroinflammation in Long COVID
Clinical Summary
Reference: Fujimoto et al., Brain Communications (2025). [¹¹C]K-2 PET shows increased AMPAR availability in cognitive long-COVID; immune signature ↑TNFSF12, ↓CCL2.
Relevance: Post-viral neuroinflammation, cognitive inefficiency, brain fog, sensory overload, POTS/IST; low CCL2; PEM; malnutrition.
Mechanism: Immune signaling → AMPAR trafficking → excess glutamatergic throughput → cognitive slowing/fatigue; may amplify autonomic instability.
Next steps:
- Diagnostic: Objective cognitive metrics; consider research AMPAR PET; trend TNFSF12/CCL2.
- Therapeutic (discuss): Perampanel (off-label) or memantine; autonomic care & pacing; track outcomes.
- Research: Neuroimmunology/post-COVID programs; longitudinal biomarkers.
In Plain English
- Your brain’s “excitatory volume knob” (AMPA receptors) looks turned up in long-COVID brain-fog.
- When that knob is high, signals fire too hard for too long — thinking slows, noise/light feel harsh, energy drains fast.
- Your labs (low CCL2) and documented neuroinflammation match the pattern in the study.
- Ask about objective memory/attention testing, research-center imaging, and medicines that gently turn the knob down (with your team).
- We’ll track function before/after any change to see what truly helps.
Source: Fujimoto et al., Brain Communications (2025). Prepared for: Nichole Anderson. This summary is educational and not medical advice.