Genetic ablation of Gpnmb does not alter synuclein-related pathology.
Alpha synuclein
GPNMB
Genetics
Parkinson's disease
Phagocytosis
eQTL
Journal
Neurobiology of disease
ISSN: 1095-953X
Titre abrégé: Neurobiol Dis
Pays: United States
ID NLM: 9500169
Informations de publication
Date de publication:
11 2021
11 2021
Historique:
received:
14
03
2021
revised:
03
08
2021
accepted:
26
08
2021
pubmed:
1
9
2021
medline:
5
3
2022
entrez:
31
8
2021
Statut:
ppublish
Résumé
The gene GPNMB is known to play roles in phagocytosis and tissue repair, and is upregulated in microglia in many mouse models of neurodegenerative disease as well as in human patients. Nearby genomic variants are associated with both elevated Parkinson's disease (PD) risk and higher expression of this gene, suggesting that inhibiting GPNMB activity might be protective in Parkinson's disease. We tested this hypothesis in three different mouse models of neurological diseases: a remyelination model and two models of alpha-synuclein pathology. We found that Gpnmb deletion had no effect on histological, cellular, behavioral, neurochemical or gene expression phenotypes in any of these models. These data suggest that Gpnmb does not play a major role in the development of pathology or functional defects in these models and that further work is necessary to study its role in the development or progression of Parkinson's disease.
Identifiants
pubmed: 34464706
pii: S0969-9961(21)00243-6
doi: 10.1016/j.nbd.2021.105494
pii:
doi:
Substances chimiques
Eye Proteins
0
GPNMB protein, human
0
Gpnmb protein, mouse
0
Membrane Glycoproteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
105494Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.