Inflammation in Alzheimer's disease (AD) is a complex area of research, with evidence showing activation of inflammatory pathways in AD brains and a potential link between inflammation and AD risk. While the exact role of inflammation as a cause, contributor, or secondary phenomenon in AD remains unclear, studies have shown that inflammation may both promote and protect against AD pathology. Microglia, the brain's resident macrophages, play a critical role in innate immune responses and can be activated by aggregated amyloid-β (Aβ) deposits. They can either remove pathogens and debris or contribute to neurodegeneration through the release of pro-inflammatory factors. Astrocytes, another key cell type, also respond to Aβ and can contribute to neuroinflammation by expressing inflammatory mediators. Oligodendrocytes and myelin are also affected by Aβ, leading to demyelination and neurodegeneration. Neurons express molecules that protect against inflammatory attack, but these protective mechanisms are often impaired in AD. The complement system, a key inflammatory pathway, is activated in AD and may contribute to both the clearance of degenerating cells and the promotion of unwanted inflammation. Cytokines, chemokines, and other soluble signaling proteins are also involved in AD, with some showing beneficial effects in mouse models. Toll-like receptors (TLRs) and other pattern recognition receptors are involved in detecting pathogens and triggering immune responses, and their activation can influence Aβ clearance and neurodegeneration. Cyclooxygenases (COX) and arachidonic acid metabolites are involved in inflammation and have been linked to AD risk. Genetic studies have identified polymorphisms in genes such as clusterin and CR1 as potential risk factors for AD, with the complement system playing a central role. Clinical studies have shown that long-term use of anti-inflammatory drugs may reduce AD risk, but treatment trials have been disappointing. The role of inflammation in AD is complex, with both protective and harmful effects, and further research is needed to develop effective therapies. Overall, inflammation is a multifaceted aspect of AD, with both harmful and beneficial roles, and understanding its mechanisms is crucial for developing new treatments.Inflammation in Alzheimer's disease (AD) is a complex area of research, with evidence showing activation of inflammatory pathways in AD brains and a potential link between inflammation and AD risk. While the exact role of inflammation as a cause, contributor, or secondary phenomenon in AD remains unclear, studies have shown that inflammation may both promote and protect against AD pathology. Microglia, the brain's resident macrophages, play a critical role in innate immune responses and can be activated by aggregated amyloid-β (Aβ) deposits. They can either remove pathogens and debris or contribute to neurodegeneration through the release of pro-inflammatory factors. Astrocytes, another key cell type, also respond to Aβ and can contribute to neuroinflammation by expressing inflammatory mediators. Oligodendrocytes and myelin are also affected by Aβ, leading to demyelination and neurodegeneration. Neurons express molecules that protect against inflammatory attack, but these protective mechanisms are often impaired in AD. The complement system, a key inflammatory pathway, is activated in AD and may contribute to both the clearance of degenerating cells and the promotion of unwanted inflammation. Cytokines, chemokines, and other soluble signaling proteins are also involved in AD, with some showing beneficial effects in mouse models. Toll-like receptors (TLRs) and other pattern recognition receptors are involved in detecting pathogens and triggering immune responses, and their activation can influence Aβ clearance and neurodegeneration. Cyclooxygenases (COX) and arachidonic acid metabolites are involved in inflammation and have been linked to AD risk. Genetic studies have identified polymorphisms in genes such as clusterin and CR1 as potential risk factors for AD, with the complement system playing a central role. Clinical studies have shown that long-term use of anti-inflammatory drugs may reduce AD risk, but treatment trials have been disappointing. The role of inflammation in AD is complex, with both protective and harmful effects, and further research is needed to develop effective therapies. Overall, inflammation is a multifaceted aspect of AD, with both harmful and beneficial roles, and understanding its mechanisms is crucial for developing new treatments.