Hypothesis Calcitonin gene-related peptide-induced central sensitization: A hypothesis for long COVID symptoms, 2025, Ella J. Lee et al

[forestglip]

Calcitonin gene-related peptide-induced central sensitization: A hypothesis for long COVID symptoms

Ella J. Lee, Cynthia Tsang, Martha Lucía Gutiérrez Pérez, Mehdi Abouzari, Hamid R. Djalilian

Abstract
Central sensitization (CS) denotes aberrant processing of sensory stimuli within the central nervous system, wherein innocuous inputs activate pain pathways, leading to pain hypersensitivity. Features observed in CS conditions are often present in patients with long COVID, suggesting a potentially shared pathophysiological mechanism.

We hypothesize that elevated levels of calcitonin gene-related peptide (CGRP), a neuropeptide known to play an integral role in the development of CS, may contribute to the persistent symptoms observed in long COVID. This article explores the role of CGRP within the context of CS and proposes its potential relationship to long COVID.

Link (Medical Hypotheses) [Paywall]

 

[Yann04]

central sensitization

 

[Nightsong]

Ahh, an overbroad conception of "central sensitisation" again.

It's not completely implausible that CGRP might play a role but a variety of medications targeting CGRP have been introduced in the last few years for migraine, including monoclonal antibodies like erenumab, and a group of small-molecule CGRP antagonists mainly given as migraine abortives (the -gepants) and if they had any effect on ME/CFS I think we would know by now (even I've tried several of them under the care of an NHS headache clinic, and they've been available for longer in private clinics and I think in the US as well). There are also other neuropeptides worthy of further research - e.g. PACAP (pituitary adenylate cyclase activating polypeptide) which also appears to be implicated in migraine pathophysiology.

(Haven't yet read beyond the abstract.)