ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026
Non-neuronal targets for migraine therapy.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- New Directions in Migraine Pathophysiology: The Glymphatic System and PACAP.Life (Basel, Switzerland) · 2026Review
- The evolving landscape of primary headache therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Migraine is a highly prevalent and severe neurological condition characterized by disabling headache attacks accompanied by other neurological symptoms. Its pathophysiology involves activation of the trigeminovascular system, cortical spreading depolarization, and dysregulation of brainstem and diencephalic nuclei. Although most studies have focussed mainly on the role of neurons, there is mounting evidence that non-neuronal cells could also participate in migraine pathophysiology and could represent targets for current and future therapies. As reviewed in this manuscript, preclinical evidence links astrocytes, microglia and satellite glial cells with cortical spreading depolarization, trigeminovascular activation, and the development of orofacial allodynia, processes that are central to migraine. These cells could be potential targets for calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating peptide (PACAP) therapies. Schwann cells have been less studied, but existing data suggest they could be targeted by anti-CGRP treatments. Macrophages respond to CGRP, contribute to cortical spreading depolarization and orofacial mechanical allodynia, and may be modulated to enhance an anti-inflammatory environment. Mast cells express receptors for CGRP and other relevant neuropeptides, and have gained attention through the development of monoclonal antibodies against their protease-activated receptor 2 (PAR2), currently in phase 2 clinical trials. Further studies are needed to better elucidate the molecular complexity of non-neuronal cells and their role in migraine, but future approaches using adeno-associated viral vectors, nanoparticles, and cell replacement strategies could enable the development of innovative anti-migraine therapies.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.