Abstract
Cardiogenic dementia (CD), recognized since the late 1970s, manifests as altered consciousness and cognition due to heart conditions. Its elusive molecular mechanisms present diagnostic and management challenges. Emerging research implicates ryanodine receptor type 2 (RyR2) mediated intracellular Ca2 + leaks in myocardial infarction (MI)-linked cognitive impairment. We hypothesize that intravenous delivery of neuron-targeted exosomes loaded with RyR2-targeting siRNA (si-RyR2) to cerebral regions could rectify Ca2 + imbalance, curbing neurotoxic protein generation tied to CD. To investigate, si-RyR2 exosomes will be administered to MI-induced mice, with hippocampal samples analyzed for Ca2 + levels, β-amyloid, and p-tau. Results hold promise for advancing CD treatment insights.
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