Neuroinflammation of Microglial Regulation in Alzheimer's Disease: Therapeutic Approaches Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive memory and cognitive decline. The pathogenesis of AD is complex, with neuroinflammation, particularly microglial activation, playing a key role in increasing disease risk, triggering onset, and accelerating progression. Modulating microglial activation and energy metabolism are promising strategies for AD treatment. Anti-inflammatory drugs and microglia-targeting therapies are emerging as new research areas. This review explores the role of microglial regulation in AD, the connection between microglial energy metabolism and AD, and advances in anti-inflammatory and microglia-regulating therapies. AD is characterized by amyloid beta (Aβ) plaques and neurofibrillary tangles (NFTs) due to tau protein hyperphosphorylation. Neuroinflammation, driven by microglial activation, is closely linked to AD pathology. Microglia can be polarized into 'M1' (pro-inflammatory) or 'M2' (anti-inflammatory) phenotypes. Excessive 'M1' activation leads to neuroinflammation, neuronal damage, and disease progression. Microglial energy metabolism is also crucial, with glycolysis playing a key role in neuroinflammation and AD pathology. Anti-inflammatory drugs, including NSAIDs, TLR4 antagonists, p38 MAPK inhibitors, and microglia regulators, are being investigated for AD treatment. These drugs target neuroinflammation, modulate microglial polarization, and regulate energy metabolism. Chinese herbal polysaccharides also show potential in neuroprotection and anti-inflammatory effects. Despite progress, challenges remain in developing effective therapies for AD. In conclusion, microglial activation and energy metabolism are critical factors in AD pathogenesis. Targeting neuroinflammation through anti-inflammatory drugs and microglia regulation offers promising therapeutic approaches for AD treatment. Further research is needed to develop effective strategies for AD prevention and treatment.Neuroinflammation of Microglial Regulation in Alzheimer's Disease: Therapeutic Approaches Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive memory and cognitive decline. The pathogenesis of AD is complex, with neuroinflammation, particularly microglial activation, playing a key role in increasing disease risk, triggering onset, and accelerating progression. Modulating microglial activation and energy metabolism are promising strategies for AD treatment. Anti-inflammatory drugs and microglia-targeting therapies are emerging as new research areas. This review explores the role of microglial regulation in AD, the connection between microglial energy metabolism and AD, and advances in anti-inflammatory and microglia-regulating therapies. AD is characterized by amyloid beta (Aβ) plaques and neurofibrillary tangles (NFTs) due to tau protein hyperphosphorylation. Neuroinflammation, driven by microglial activation, is closely linked to AD pathology. Microglia can be polarized into 'M1' (pro-inflammatory) or 'M2' (anti-inflammatory) phenotypes. Excessive 'M1' activation leads to neuroinflammation, neuronal damage, and disease progression. Microglial energy metabolism is also crucial, with glycolysis playing a key role in neuroinflammation and AD pathology. Anti-inflammatory drugs, including NSAIDs, TLR4 antagonists, p38 MAPK inhibitors, and microglia regulators, are being investigated for AD treatment. These drugs target neuroinflammation, modulate microglial polarization, and regulate energy metabolism. Chinese herbal polysaccharides also show potential in neuroprotection and anti-inflammatory effects. Despite progress, challenges remain in developing effective therapies for AD. In conclusion, microglial activation and energy metabolism are critical factors in AD pathogenesis. Targeting neuroinflammation through anti-inflammatory drugs and microglia regulation offers promising therapeutic approaches for AD treatment. Further research is needed to develop effective strategies for AD prevention and treatment.