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Alzheimer's disease (AD) is the most common type of dementia and a neurodegenerative disorder. Histopathologically, two significant hallmarks, intracellular neurofibrillary tangles (NFTs) and extracellular neuritic plaques (NPs) enclosed by initiated astrocytes and microglia, define the disease. NFTs are made up of paired helical filaments of hyperphosphorylated fragment tau protein. The amyloid-peptide (Aβ), a small fragment of 50–52 amino acids with a molecular weight of 5 kD, is the primary aspect of the NP. It has been suggested that amyloid materials and microglia activation can promote the neurodegenerative process seen in Alzheimer's disease patients. However, the role of inflammation in Alzheimer's disease is debatable. In the early stages of the disease, inflammation may play a beneficial role in pathology, as activated microglia and astrocytes are thought to be involved in Aβ clearance.Nonetheless, chronic microglia signaling has been linked to increases in Aβ and potentially tau phosphorylation. Complement molecules, pro-inflammatory cytokines, acute inflammatory reactants, and other inflammatory mediators are upregulated in AD brains, possibly contributing to the neurodegenerative process. Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown in clinical studies and animal models to reduce the risk of getting AD and reduce A accumulation. Eventually, more study is needed to find whether anti-inflammatory strategies can slow the neurodegenerative method which impacts such patients.