Lack of association between TREM2 rs75932628 variant and amyotrophic lateral sclerosis.
Amyotrophic lateral sclerosis
Genetic variant
Genetics
TREM2
rs75932628
Journal
Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234
Informations de publication
Date de publication:
Mar 2021
Mar 2021
Historique:
received:
09
02
2021
accepted:
20
03
2021
pubmed:
8
4
2021
medline:
20
5
2021
entrez:
7
4
2021
Statut:
ppublish
Résumé
Amyotrophic lateral sclerosis (ALS) is a multifactorial neurodegenerative disease. Inflammatory processes are among the mechanisms that are implicated in ALS pathogenesis. The TREM2 rs75932628 T variant may influence the regulatory effect of TREM2 on inflammation. Studies regarding the role of the rs75932628 variant in ALS have yielded inconsistent results, so far. To assess the role of TREM2 rs75932628 on ALS risk. We genotyped 155 patients with sporadic ALS and 155 healthy controls for TREM2 rs75932628. We also merged and meta-analyzed our data with data from previous studies (with a total of 7524 ALS cases and 14,675 controls), regarding TREM2 rs75932628 and ALS. No ALS or healthy subjects carried the TREM2 rs75932628-T variant. Results from meta-analyses (overall approach and sensitivity analyses) yielded no significant results for possible connection between TREM2 rs75932628-T variant and ALS. Based on our results, TREM2 rs75932628 does not seem to play a determining role to the pathophysiology of ALS.
Identifiants
pubmed: 33826063
doi: 10.1007/s11033-021-06312-1
pii: 10.1007/s11033-021-06312-1
doi:
Substances chimiques
Membrane Glycoproteins
0
Receptors, Immunologic
0
TREM2 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2601-2610Subventions
Organisme : This study was supported in part by a research grant from the Research Committee of the University of Thessaly, Greece (code: 5287).
ID : code: 5287
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