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GSK3β genetic variability in patients with Multiple Sclerosis
Daniela Galimberti1, James Macmurray, Diego Scalabrini
1Department of Neurological Sciences, "Dino Ferrari" Center, University of Milan, Fondazione Cà Granda, IRCCS Ospedale Maggiore Policlinico, Milan, Italy. daniela.galimberti@unimi.it
Abstract:
Glycogen synthase kinase-3 beta (GSK3β) is a ubiquitous kinase that is part of multiple signaling pathways. It has neurotrophic/neuroprotective effects by mediating the actions of neurotrophic molecules in the brain, thus providing neuroprotection through modulation of energy metabolism. Notably, it has been demonstrated that GSK3β is involved in Wnt-beta-catenin signaling, which contributes to the inhibition of myelination and remyelination processes in mammals. Three-hundred nineteen patients with MS and 294 age-matched controls were genotyped by allelic discrimination for four common GSK3β variants (rs2199503, rs9826659, rs334558 and rs6438552) tagging about 100% of GSK-3β variability. A statistically significant increased frequency of the rs334558 GG genotype was observed in patients as compared with controls (25.4% versus 17.7%, P=0.02; OR:1.58, 95%CI: 1.07-2.34). Stratifying MS patients according to the disease subtype, a statistically significant difference of rs334558 GG frequency was found between Relapsing Remitting (RR), but not Primary Progressive or Secondary MS, and controls (27.0% versus 17.7%, P=0.01; OR: 1.72, 95%CI: 1.13-2.61). GSK3β rs334558 is a susceptibility factor for MS. As it is located in the promoter region, a possible explanatory mechanism could be an influence of the variant on the gene transcription rate.
Insights
Genetic variations in Glycogen synthase kinase-3 beta (GSK3β) were studied in multiple sclerosis (MS). A specific GSK3β variant (rs334558 GG) was found to increase MS susceptibility, particularly in the Relapsing Remitting subtype.
Area of Science:
- Neuroscience
- Genetics
- Immunology
Background:
- Glycogen synthase kinase-3 beta (GSK3β) plays a role in neuroprotection and energy metabolism.
- GSK3β is implicated in Wnt-beta-catenin signaling, affecting myelination and remyelination processes.
- Dysregulation of GSK3β signaling is potentially linked to neurological disorders like multiple sclerosis (MS).
Purpose of the Study:
- To investigate the association between common Glycogen synthase kinase-3 beta (GSK3β) variants and susceptibility to multiple sclerosis (MS).
- To determine if specific GSK3β genotypes influence MS risk or disease subtypes.
Main Methods:
- Genotyping of 319 MS patients and 294 controls for four common GSK3β variants (rs2199503, rs9826659, rs334558, rs6438552).
- Allelic discrimination method used for genotyping.
- Statistical analysis to compare genotype frequencies between MS patients and controls, including stratification by MS subtype.
Main Results:
- A statistically significant increase in the rs334558 GG genotype frequency was observed in MS patients compared to controls (25.4% vs. 17.7%, P=0.02).
- This association remained significant when stratifying by MS subtype, with a higher frequency of the rs334558 GG genotype in Relapsing Remitting MS patients (27.0% vs. 17.7%, P=0.01).
- The rs334558 variant, located in the promoter region, may influence gene transcription rates.
Conclusions:
- The GSK3β rs334558 variant is identified as a susceptibility factor for multiple sclerosis.
- This genetic variation may contribute to MS pathogenesis, potentially through altered GSK3β gene expression.
- Further research is warranted to elucidate the precise mechanisms linking GSK3β variants to MS development.
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