Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and two core pathologies: amyloid β plaques and neurofibrillary tangles (NFTs). Over the past decade, sustained immune responses in the brain have been identified as a third core pathology, with microglia activation exacerbating both amyloid and tau pathologies. This review highlights the role of inflammation in AD, focusing on microglia-related signaling mechanisms, cytokines, and the potential link between AD risk factors and inflammatory mechanisms. Microglia, the brain's resident immune cells, play a critical role in clearing amyloid β, but prolonged activation leads to chronic neuroinflammation, worsening AD pathology. The TREM2 receptor, associated with increased AD risk, is involved in microglial function and regulation of inflammation. Other microglial receptors, such as CX3CR1 and GABA_B, also contribute to neuroinflammation and AD progression. Pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6, as well as anti-inflammatory cytokines like IL-10 and TGF-β1, are central to AD pathogenesis. Inflammation is also linked to AD risk factors such as diabetes and cardiovascular disease. Understanding these inflammatory mechanisms is crucial for developing therapeutic strategies targeting AD.Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and two core pathologies: amyloid β plaques and neurofibrillary tangles (NFTs). Over the past decade, sustained immune responses in the brain have been identified as a third core pathology, with microglia activation exacerbating both amyloid and tau pathologies. This review highlights the role of inflammation in AD, focusing on microglia-related signaling mechanisms, cytokines, and the potential link between AD risk factors and inflammatory mechanisms. Microglia, the brain's resident immune cells, play a critical role in clearing amyloid β, but prolonged activation leads to chronic neuroinflammation, worsening AD pathology. The TREM2 receptor, associated with increased AD risk, is involved in microglial function and regulation of inflammation. Other microglial receptors, such as CX3CR1 and GABA_B, also contribute to neuroinflammation and AD progression. Pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6, as well as anti-inflammatory cytokines like IL-10 and TGF-β1, are central to AD pathogenesis. Inflammation is also linked to AD risk factors such as diabetes and cardiovascular disease. Understanding these inflammatory mechanisms is crucial for developing therapeutic strategies targeting AD.