Worst spasticity in patients post-stroke associated with MNSOD ALA16VAL polymorphism and interleukin-1β

Area of Science:

• Genetics and Neurology
• Molecular Biology
• Vascular Disease Research

Background:

• The MnSOD Ala16Val single nucleotide polymorphism (SNP) is linked to metabolic and vascular disease risk.
• Its specific role in stroke, particularly concerning spasticity, remains largely unexplored.
• Stroke presents with neurological deficits, including motor impairments and spasticity.

Purpose of the Study:

• To investigate the association between the MnSOD Ala16Val SNP and spasticity in stroke patients.
• To examine the SNP's influence on interleukin (IL) levels, brain-derived neurotrophic factor (BDNF), and glycolipid parameters.
• To explore potential correlations between these markers and stroke-related spasticity.

Main Methods:

• Study included 80 post-stroke subjects and 80 healthy controls.
• Genotyping for the MnSOD Ala16Val SNP was performed.
• Analysis of spasticity, IL-1β, IL-6, INF-γ, BDNF, total cholesterol, LDL, triglycerides, glucose, and caspase activation was conducted.
• DNA damage assessment was also performed.

Main Results:

• The VV genotype group exhibited higher spasticity, total cholesterol, LDL, IL-1β, IL-6, and INF-γ levels.
• A significant correlation was found between IL-1β levels and spasticity in the VV post-stroke group.
• Triglycerides, glucose, and caspase activation were elevated, while BDNF levels were reduced in both VV and AV post-stroke groups.
• Increased DNA damage was observed in the overall post-stroke group.

Conclusions:

• The V allele of the MnSOD Ala16Val SNP is associated with an unfavorable glycolipid profile, potentially disrupting neurovascular homeostasis.
• Elevated inflammatory markers and reduced BDNF levels in VV genotype patients may contribute to stroke incidence and severity, particularly spasticity.
• These findings suggest the MnSOD Ala16Val SNP influences stroke pathophysiology and clinical outcomes related to spasticity.