Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Exploring Novel Therapeutic Targets in the Common Pathogenic Factors in Migraine and Neuropathic Pain

Version 1 : Received: 31 December 2022 / Approved: 4 January 2023 / Online: 4 January 2023 (01:53:45 CET)

A peer-reviewed article of this Preprint also exists.

Tajti, J.; Szok, D.; Csáti, A.; Szabó, Á.; Tanaka, M.; Vécsei, L. Exploring Novel Therapeutic Targets in the Common Pathogenic Factors in Migraine and Neuropathic Pain. Int. J. Mol. Sci. 2023, 24, 4114. Tajti, J.; Szok, D.; Csáti, A.; Szabó, Á.; Tanaka, M.; Vécsei, L. Exploring Novel Therapeutic Targets in the Common Pathogenic Factors in Migraine and Neuropathic Pain. Int. J. Mol. Sci. 2023, 24, 4114.

Abstract

Migraine and neuropathic pain (NP) are evocative of painful, disabling, chronic conditions which exhibit resembling symptoms and thus considered to share a common etiology. Calcitonin gene-related peptide (CGRP) has gained credit as a target for migraine management; nevertheless, the efficacy and the applicability of CGRP modifiers warrant search for more effective therapeutic targets for pain management. This scoping review overviews human studies of common pathogenic factors in migraine and NP to explore potential novel therapeutic targets. CGRP causes inflammation in the meninges; monoclonal antibodies and inhibitors target CGRP. Gluta-mate-induced hyperexcitability and subsequent sensitization are closely linked to an alteration of the tryptophan (Trp)-kynurenine (KYN) metabolic system; the Trp-KYN system may serve as a potential target. Microglial overaction is observed in migraine and NP; modifying the microglial activity may be a possible approach. Cytokine-induced inflammation is a leading hypothesis of the pathogenesis of the conditions; alleviating neuroinflammation may complement a pain-relieving armamentarium. Transient receptor potential (TRP) ion channels evoke the release of several substances; TRP ion channels may potentially emerge as new targets. The endocannabinoid system plays a major role in the pain trafficking pathway; modification of the system may open a new path toward discovery of new analgesics. Here we highlight the mechanism of those common pathogenic factors to explore therapeutic targets for innovative pain management in migraine and NP.

Keywords

migraine; neuropathic pain; calcitonin gene-related peptide (CGRP); kynurenine; glia; cytokines; neuroinflammation; transient receptor potential (TRP) ion channels; endocannabinoids

Subject

Medicine and Pharmacology, Neuroscience and Neurology

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.

Leave a public comment
Send a private comment to the author(s)
* All users must log in before leaving a comment
Views 0
Downloads 0
Comments 0
Metrics 0


×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.
We use cookies on our website to ensure you get the best experience.
Read more about our cookies here.