Autor(es)

Goncalves, Fernanda de Toledo ; Marques, Lucas Murrins ; Pessotto, Anne Victorio ; Barbosa, Sara Pinto ; Imamura, Marta ; Simis, Marcel ; Fregni, Felipe ; Battistella, Linamara

• Tipo de documento: Artigo Científico
• Fonte: NEUROPHYSIOLOGIE CLINIQUE-CLINICAL NEUROPHYSIOLOGY; v. 53, n. 6, p. 9-pg., 2023-11-07.

Resumo

Objective: The present study investigated the relationship between three genetic polymor-phisms of OPRM1 (rs1799971 -A118G and rs1799972 -C17T) and BDNF (rs6265 -C196T) and EEG-measured brain oscillations in Knee Osteoarthritis (KOA) patients.Materials and Methods: We performed a cross-sectional analysis of a cohort study (DEFINE cohort), KOA arm, with 66 patients, considering demographic (age, sex, and education), clinical (pain intensity and duration), OPRM1 (rs1799971 -A118G and rs1799972 -C17T) and BDNF (rs6265 -C196T) genotypes, and electrophysiological measures. Brain oscillations relative power from Delta, Theta, Alpha, Low Alpha, High Alpha, Beta, Low Beta and High Beta oscillations were measured during resting state EEG. Multivariate regression models were used to explore the main brain oscillation predictors of the three genetic polymorphisms.Results: Our findings demonstrate that Theta and Low Beta oscillations are associated with the variant allele of OPRM1-rs1799971 (A118G) on left frontal and left central regions, respectively, while Alpha brain oscillation is associated with variant genotypes (CT/TT) of BDNF-rs6265 on frontal (decrease of oscillation power) and left central (increase of oscillation power) regions. No significant model was found for OPRM1-rs1799972 (C17T) in addition to the inclusion of pain intensity as a significant predictor of this last model.Conclusion: One potential interpretation for these findings is that polymorphisms of OPRM1 that is involved with endogenous pain control lead to increased compensatory oscillatory mechanisms, characterized by increased theta oscillations. Along the same line, polymorphisms of the BDNF lead to decreased alpha oscillations in the frontal area, likely also reflecting the disruption of resting states to also compensate for the increased injury associated with knee OA. It is possible that these polymorphisms require additional brain adaption to the knee OA related injury.(c) 2023 Published by Elsevier Masson SAS. (AU)

• Processo FAPESP: 17/12943-8 - O déficit da inibição como marcador de neuroplasticidade na reabilitação
• Beneficiário: Felipe Fregni
• Modalidade de apoio: Auxílio à Pesquisa - Programa SPEC
• Processo FAPESP: 20/08512-4 - O déficit da inibição como marcador de neuroplasticidade na reabilitação
• Beneficiário: Sara Barbosa Franco
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 20/14028-8 - Análise crítica da utilização do banco de dados digital para a coleta de dados dos pacientes amputados do estudo inhibitory deficit as a marker of neuroplasticity in rehabilitation
• Beneficiário: Anne Victório Pessotto
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• Processo FAPESP: 21/05897-5 - O déficit da inibição como marcador de neuroplasticidade na reabilitação
• Beneficiário: Lucas Murrins Marques
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado