Uncovering a Genetic Polymorphism Located in Huntingtin Associated Protein 1 in Modulation of Central Pain Sensitization Signaling Pathways.
GWAS
HAP1
central sensitization
fibromyalgia
nociceptive flection reflex (NFR) threshold
Journal
Frontiers in neuroscience
ISSN: 1662-4548
Titre abrégé: Front Neurosci
Pays: Switzerland
ID NLM: 101478481
Informations de publication
Date de publication:
2022
2022
Historique:
received:
02
11
2021
accepted:
27
05
2022
entrez:
15
7
2022
pubmed:
16
7
2022
medline:
16
7
2022
Statut:
epublish
Résumé
Fibromyalgia syndrome (FMS) is characterized by widespread pain and increased sensitivity to nociceptive stimulus or tenderness. While familial aggregation could suggest a potential hereditary component in FMS development, isolation of genetic determinants has proven difficult due to the multi-factorial nature and complexity of the syndrome. Central sensitization is thought to be one of the key mechanisms leading to FMS in a subset of patients. Enhanced central pain signaling can be measured using the Nociceptive Flexion Reflex (NFR) or RIII threshold. We performed a genome-wide association study (GWAS) using an array to genotype 258,756 human genetic polymorphisms in 225 FMS patients and 77 healthy volunteers and searched for genetic variants associated with a lowered NFR threshold. We have identified a potential association between a single nucleotide polymorphism resulting in a common non-synonymous coding mutation in the Huntingtin associated protein 1 (
Identifiants
pubmed: 35837121
doi: 10.3389/fnins.2022.807773
pmc: PMC9274135
doi:
Types de publication
Journal Article
Langues
eng
Pagination
807773Informations de copyright
Copyright © 2022 Gloor, Matthey, Sobo, Mouterde, Kosek, Pickering, Poloni, Cedraschi, Ehret and Desmeules.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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