Alzheimer's disease (AD) is a complex and heterogeneous condition characterized by the presence of extracellular amyloid-β (Aβ) plaques and intracellular hyperphosphorylated tau tangles. Despite significant advancements in understanding AD pathobiology, no disease-modifying treatments are currently available. Recent studies have highlighted the roles of other cellular and molecular processes, such as neuroinflammation and tau accumulation, which may be more critical drivers of neurodegeneration. The article reviews recent advances in AD pathobiology, including the involvement of Aβ aggregation, tau pathology, ApoE isoforms, and neuroimmune activation. It also discusses the potential role of the gut microbiome and infectious agents in AD pathogenesis. The review emphasizes the need for further research to develop effective disease-modifying therapies for AD.Alzheimer's disease (AD) is a complex and heterogeneous condition characterized by the presence of extracellular amyloid-β (Aβ) plaques and intracellular hyperphosphorylated tau tangles. Despite significant advancements in understanding AD pathobiology, no disease-modifying treatments are currently available. Recent studies have highlighted the roles of other cellular and molecular processes, such as neuroinflammation and tau accumulation, which may be more critical drivers of neurodegeneration. The article reviews recent advances in AD pathobiology, including the involvement of Aβ aggregation, tau pathology, ApoE isoforms, and neuroimmune activation. It also discusses the potential role of the gut microbiome and infectious agents in AD pathogenesis. The review emphasizes the need for further research to develop effective disease-modifying therapies for AD.