This study explores the complex pathogenesis of Alzheimer’s disease (AD), emphasizing the critical roles of advanced glycation end-products (AGEs), oxidative stress, and metabolic dysfunctions. The AGE-RAGE pathway is highlighted for its contribution to neurodegeneration, amyloid-beta (Aβ) accumulation, and tau protein pathology, proposing it as a possible treatment target. Natural compounds, such as antioxidants and anti-glycative agents, offer promising neuroprotective effects by inhibiting these processes and improving cognitive function. The metabolic link between AD and type 2 diabetes further complicates disease progression, suggesting that targeting glucose metabolism could provide novel therapeutic strategies. Despite challenges such as blood-brain barrier penetration and genetic variability, future research should focus on personalized, multi-target therapies. These therapies would aim to mitigate oxidative stress, mitochondrial dysfunction, and neuroinflammation, offering hope for more effective treatments and enhanced quality of life for individuals with AD.