Molecular mechanisms of aging in the pathogenesis of Alzheimer’s disease

Alzheimer’s disease (AD) is a chronic neurodegenerative disorder and the leading cause of dementia, primarily affecting the elderly. This review explores the critical role of aging in the onset and progression of AD, emphasizing how age-related physiological changes such as oxidative stress, mitochondrial dysfunction, and diminished neuroplasticity intensify core pathological features, including amyloid-β (Aβ) aggregation, tau hyperphosphorylation, and neuroinflammation. It discusses genetic risk factors, particularly APOE variants, and their modulatory influence within the context of aging. The article highlights the intricate overlap between normal aging and AD pathology, which hinders early diagnosis and necessitates the advancement of biomarker development and imaging technologies. Furthermore, it examines how aging alters the pharmacokinetics and pharmacodynamics of therapeutic agents, underscoring the need for age-specific treatment strategies. The review advocates for a multidisciplinary approach integrating neuroscience, geriatrics, and public health to drive innovative preventive and therapeutic solutions. Addressing the aging-AD interplay is essential for curbing the growing global burden of dementia and improving life quality for aging populations.