Atrial fibrillation-induced neurocognitive and vascular dysfunction is averted by mitochondrial oxidative stress reduction.

ABSTRACT: Atrial fibrillation (AF) is a prevalent arrhythmia with known detriments such as heart failure, stroke, and cognitive decline even in patients without prior stroke. The mechanisms by which AF leads to cognitive dysfunction are yet unknown, and there is a lack of animal models to study this disease process. We previously developed a murine model of spontaneous and prolonged episodes of AF, a double transgenic mouse model with cardiac-specific expression of a gain-of-function mutant voltage-gated sodium channel (DTG-AF mice). Herein, we show, for the first time to our knowledge, a murine model of AF without any cerebral infarcts exhibiting cognitive dysfunction, including impaired visual learning and cognitive flexibility on touch screen testing. Mesenteric resistance arterial function of DT

SUBMITTER: Guttipatti P 

PROVIDER: S-EPMC12643510 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature