Translating Molecular Pathogenesis into Therapeutics: Emerging Strategies and Clinical Prospects for Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is a devastating neurodegenerative disorder that affects millions of people worldwide and poses a major global health challenge. This complex disease involves multiple pathogenic factors, including amyloid-beta (Aβ), tau protein aggregation, synaptic dysfunction, mitochondrial impairment, oxidative stress, and genetic influences. While the intricate interplay and individual contributions of these elements to AD progression remain under investigation, considerable advancements have been made in elucidating their roles. This review examines the molecular mechanisms underlying the pathogenesis of AD, highlighting how each factor contributes to the onset and progression of the disorder. To date, significant efforts in AD research have focused on diverse therapeutic approaches, including targeting Aβ and tau proteins, modulating neuroinflammation, enhancing autophagy, and restoring synaptic function. As these strategies evolve, they provide renewed hope for interventions that could slow AD progression and improve cognitive function. Furthermore, a multi-targeted approach addressing these interconnected pathways shows promise for managing the complex pathology of AD. Continued research in these areas will be essential for identifying novel therapeutic options and advancing clinical strategies for AD management.