A serious, long-term degenerative neurological disease in humans is one definition of Alzheimer’s disease (AD). AD brain areas that are pathologically sensitive exhibit inflammation, and this inflammation carries with it all the complexity of peripheral local inflammatory responses. Degenerating tissue and the buildup of very insoluble aberrant materials are two traditional causes of peripheral inflammation. Nowadays, the inhibitors which were discovered before cannot have a good effect on the treatment to the growth of this disease. This article provides an overview of how microglia-mediated neuroinflammation affects AD, with particular attention to the pathogenic process of microglia, and the potential and recent developments in neuroinflammation as an AD diagnostic and treatment target. Therefore, even if clinical research and animal models are still in their infancy, they clearly imply that AD inflammation plays a major role in AD pathogenesis. Gaining more insight into the immunoregulatory and inflammatory mechanisms underlying AD should make it feasible to create anti-inflammatory treatments that, while probably not curative, will at least assist postpone the start or decrease the disease’s terrible course.
