Mitochondrial-Targeted Small Molecules: A Promising Approach for Alzheimer’s Disease Treatment and Neuroprotection

Abstract

Alzheimer’s disease (AD) is a debilitating neurodegenerative condition characterized by memory loss, cognitive decline, and personality changes. Recent research has shed light on the critical role of mitochondria in AD pathogenesis, specifically their involvement in the production and aggregation of amyloid-beta (Aβ) and phosphorylated tau. Mitochondrial dysfunction is a hallmark of AD, with reactive oxygen species (ROS) playing a central role. Oxidative stress resulting from mitochondrial ROS production is closely linked to AD’s early pathogenesis. Furthermore, the interaction between phosphorylated tau and Aβ disrupts mitochondrial function, hindering energy production and leading to synaptic dysfunction. This article explores the promising advancements in mitochondria-targeted small molecules as potential treatments for AD.