Alzheimer’s disease (AD) is a chronic, progressive neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) plaques and hyperphosphorylated Tau, leading to neurofibrillary tangle formation and synaptic dysfunction. Increasing evidence indicates that these hallmark pathologies are shaped by sustained alterations in neuroimmune and metabolic homeostasis. Lifestyle-associated exposures, including ethanol consumption and high-fat diet (HFD) intake, are emerging as modulators of