Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and the presence of two core pathologies: amyloid β plaques and neurofibrillary tangles. Over the past decade, a sustained immune response in the brain has emerged as a third core pathology in AD. This review provides an overview of inflammation in AD and a detailed coverage of microglia-related signaling mechanisms implicated in AD. It also reviews the potential connection between risk factors for AD and their relation to inflammatory mechanisms. The review highlights the role of microglia in AD, including their activation, cytokine production, and the involvement of specific receptors such as TREM2, CX3CR1, and GABA_B. Additionally, it discusses the impact of specific cytokines like TNF-α, IL-1β, IL-6, NFκB, IL-10, and TGF-β1 on AD pathology. The relevance of inflammation and risk factors for AD, such as diabetes mellitus and ApoE, is also explored. The review emphasizes the need for further research into therapeutic approaches targeting the sustained inflammatory response in AD.Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and the presence of two core pathologies: amyloid β plaques and neurofibrillary tangles. Over the past decade, a sustained immune response in the brain has emerged as a third core pathology in AD. This review provides an overview of inflammation in AD and a detailed coverage of microglia-related signaling mechanisms implicated in AD. It also reviews the potential connection between risk factors for AD and their relation to inflammatory mechanisms. The review highlights the role of microglia in AD, including their activation, cytokine production, and the involvement of specific receptors such as TREM2, CX3CR1, and GABA_B. Additionally, it discusses the impact of specific cytokines like TNF-α, IL-1β, IL-6, NFκB, IL-10, and TGF-β1 on AD pathology. The relevance of inflammation and risk factors for AD, such as diabetes mellitus and ApoE, is also explored. The review emphasizes the need for further research into therapeutic approaches targeting the sustained inflammatory response in AD.