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

Gene

Centro de Ciências da Saúde, Departamento de Neuropsiquiatria, Universidade Federal de Santa Maria, RS, Brazil; Centro de Ciências Naturais e Exatas, Programa de Pós-graduação em Ciências Biológicas: Bioquímica Toxicológica, Universidade Federal de Santa Maria, RS, Brazil; Centro de Educação Física e Desportos, Laboratório de Bioquímica do Exercício (BIOEX), Universidade Federal de Santa Maria, RS, Brazil; Centro de Ciências da Saúde, Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria, RS, Brazil. Electronic address:

Published: December 2022

The MnSOD Ala16Val single nucleotide polymorphism (SNP) has shown to be associated to risk factors of several metabolic and vascular diseases. However, little is known about interaction between MnSOD Ala16Val SNP in stroke, a frequent neurologic disease that involves clinic manifestations such as motor deficits and spasticity. In this sense, we decided to investigate the relationship between MnSOD Ala16Val SNP with spasticity in stroke and also its influence on interleukin levels, BDNF, and glycolipid parameters. Eighty post-stroke subjects and 80 healthy controls were investigated. We showed a higher spasticity, levels of total cholesterol, LDL, IL-1β, IL-6, and INF-γ in VV post-stroke group. Interesting, we found a correlation between IL-1β levels and spasticity in VV post-stroke. Triglycerides, glucose levels and caspases (1 and 3) activation were significantly higher, as well as BDNF levels were lower in VV and AV post-stroke. DNA damage was higher in post-stroke group. Thus, we can suggest that the V allele has a worse glycolipid profile, which would facilitate changes in neurovascular homeostasis. These events associated with an increase in inflammatory markers and a reduction in BDNF can contribute with the stroke and a worse clinical evolution in relation to spasticity in patients with VV genotype.

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Source
http://dx.doi.org/10.1016/j.gene.2022.146880DOI Listing

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