| Literature DB >> 33606765 |
Jéssica Barletto de Sousa Barros1, Kamilla de Faria Santos1, Rômulo Morais Azevedo1, Rayana Pereira Dantas de Oliveira1, Ana Carolina Dourado Leobas1, Dhiogo da Cruz Pereira Bento2, Rodrigo da Silva Santos1, Angela Adamski da Silva Reis1.
Abstract
Amyotrophic Lateral Sclerosis (ALS) is a rare neurodegenerative disease that affects motor neurons and promotes progressive muscle atrophy. It has a multifactorial etiology, where environmental conditions playing a remarkable role through the increase of oxidative stress. Genetic polymorphisms in cell detoxification genes, such as Glutathione S-Transferase Pi 1 (GSTP1) can contribute to excessive oxidative stress, and therefore may be a risk factor to ALS. Thus, this study aimed to investigate the role of the GSTP1 rs1695 polymorphism in ALS susceptibility in different genetic inheritance models and evaluate the association of the genotypes with risk factors, clinical and demographic characteristics of ALS patients from the Brazilian central population. This case-control study was conducted with 101 patients with ALS and 101 healthy controls. GSTP1 rs1695 polymorphism genotyping was performed with Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP). The statistical analysis was carried out using the SPSS statistical package and SNPStats software. Analysis of genetic inheritance models was performed by logistic regression, which was used to determine the Odds Ratio. The results of this first study in the Brazilian population demonstrated that there was no risk association between the development of ALS and the GSTP1 rs1695 polymorphism in any genetic inheritance model (codominant, dominant, recessive, overdominant, and logarithmic); and that the polymorphic variants were not associated with the clinical and demographic characteristics of ALS patients. No association of the GSTP1 rs1695 polymorphism and ALS development in the Brazilian central population was found. These findings may be justified by the multifactorial character of the disease.Entities:
Year: 2021 PMID: 33606765 PMCID: PMC7894827 DOI: 10.1371/journal.pone.0247024
Source DB: PubMed Journal: PLoS One ISSN: 1932-6203 Impact factor: 3.240