Alzheimer's disease is a progressive neurological condition marked by neuronal degradation, memory loss, and cognitive decline. The disease's primary pathogenic features are intracellular neurofibrillary tangles made of hyperphosphorylated tau protein and extracellular amyloid-β plaque formation. Microglia are involved in both neuroprotection and neurotoxicity, and neuroinflammation has been identified as a key factor in the development of disease in recent years. Initially, microglia use phagocytosis to help remove amyloid-β and cellular debris, but prolonged activation causes oxidative stress, excessive cytokine release, chronic inflammation, and synaptic dysfunction, all of which lead to neuronal damage and cognitive impairment. The structure and function of microglia, neuroinflammatory signaling pathways, microglial activation mechanisms, and cellular interaction between microglia and astrocytes in Alzheimer's disease are all covered in this research. The review also emphasizes important therapy strategies, including as monoclonal antibodies, NMDA receptor antagonists, acetylcholinesterase inhibitors, medications that target tau and amyloid, and lifestyle-based interventions. Comprehending the molecular pathways governing neuroinflammation and microglial activation may aid in the creation of more potent Alzheimer's disease treatment approaches.
Apurva Singh (Sun,) studied this question.