Molecular docking and ADMET analysis of coenzyme Q10 as a potential therapeutic agent for Alzheimer's disease

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by cognitive decline, synaptic dysfunction, and neuroinflammation, with oxidative stress playing a crucial role. Coenzyme Q10 (CoQ10), known for its antioxidant properties, has been proposed as a potential therapeutic agent due to its ability to mitigate oxidative damage and maintain mitochondrial integrity. This study investigates the molecular interactions of CoQ10 with key proteins involved in AD pathology—Glycogen Synthase Kinase-3β (GSK-3β), Protein Kinase B (PKB), and Phosphatidylinositol-3-kinase (PI3K)—through molecular docking methods. Results indicate that CoQ10 exhibits the strongest binding affinity with GSK-3β, potentially reducing tau protein phosphorylation, a hallmark of AD. ADMET analysis further supports CoQ10’s drug-like properties, with favorable absorption and safety profiles, though limited blood-brain barrier permeability poses challenges. This in-silico study highlights CoQ10’s therapeutic potential in addressing neuroinflammation and oxidative stress in AD, warranting further in vitro and in vivo validation.

Keywords: Alzheimer’s disease, coenzyme Q10, molecular docking, oxidative stress, neuroinflammation