Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia worldwide, accounting for 60–80% of dementia cases. It is characterized by gradual cognitive decline, neuronal loss, and pathological hallmarks, including amyloid-β (Aβ) plaques and neurofibrillary tangles of hyperphosphorylated tau protein. This review provides a comprehensive overview of AD, emphasizing its etiology, molecular mechanisms, risk factors, and current therapeutic strategies. Multiple hypotheses, including the amyloid cascade, tau, cholinergic, vascular, and neuroinflammatory theories, are discussed to elucidate disease pathogenesis. Genetic mutations in the APP, PSEN1, and PSEN2 genes, along with environmental and lifestyle factors, are shown to influence disease onset and progression. The treatment landscape is rapidly evolving from traditional symptomatic therapies, such as cholinesterase inhibitors and NMDA receptor antagonists, to emerging disease-modifying agents targeting amyloid, tau, and neuroinflammation. Novel approaches, including glutaminyl cyclase inhibitors, PDE inhibitors, serotonin receptor modulators, and metabolic therapies, offer new hope for altering disease progression. Non-pharmacological interventions, such as diet, exercise, and lifestyle modifications, also play a key preventive role. Despite ongoing challenges, advancements in biomarker research, neuroimaging, and precision medicine are improving early detection and individualized treatment strategies. Continuous innovation in pharmacotherapy and diagnostics promises to reshape the future of AD management and enhance patients’ quality of life. The current review focuses on bridging the gaps in AD’s current and emerging Therapies.
Mostafa et al. (2026) studied this question.