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Its complex pathophysiology involves multiple interlinked processes, including amyloid\u2010\u03b2 (A\u03b2) aggregation, tau hyperphosphorylation, oxidative stress, neuroinflammation, synaptic dysfunction, and cholinergic deficits. Current FDA\u2010approved therapies provide only symptomatic relief and fail to halt disease progression, highlighting the urgent need for more effective treatment strategies. This review provides a comprehensive overview of the pathological mechanisms underlying AD and the emerging therapeutic targets for the design of tractable anti\u2010AD scaffolds, namely, acetylcholinesterase, beta\u2010site amyloid precursor protein cleaving enzyme 1 (BACE1), glycogen synthase kinase\u20103\u03b2 (GSK3\u03b2), dual\u2010specificity tyrosine phosphorylation\u2010regulated kinase 1A (DYRK1A), histone deacetylases (HDACs), and soluble epoxide hydrolase (sEH). 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