Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive memory and cognitive decline. The pathogenesis of AD involves the accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles (NFTs), primarily due to the hyperphosphorylation of tau protein. Microglial activation, a key component of neuroinflammation, plays a crucial role in AD by enhancing Aβ clearance and driving the spread of tau proteins. This review explores the connection between microglial energy metabolic disorders, neuroinflammation, and AD development, highlighting the potential of anti-inflammatory and microglia-regulating therapies. Microglia, the primary immune cells in the central nervous system (CNS), are involved in various physiological processes such as brain development, activity, and plasticity. They can polarize into anti-inflammatory 'M2' or pro-inflammatory 'M1' phenotypes, with the latter being associated with neuronal damage and degeneration. Chronic microglial activation leads to a vicious cycle of Aβ and tau accumulation, contributing to neurodegeneration and cognitive decline. The energy metabolic disorders of microglia, particularly the switch from oxidative phosphorylation (OXPHOS) to glycolysis, are critical in driving neuroinflammation. Pro-inflammatory cytokines and other mediators produced during glycolysis further exacerbate neuroinflammation and neuronal damage. Targeting glycolytic pathways and microglial polarization may provide new therapeutic approaches to mitigate neuroinflammation and its harmful effects. Recent advancements in anti-inflammatory drugs and microglia regulators offer promising strategies for AD treatment. Non-steroidal anti-inflammatory drugs (NSAIDs), TLR4 antagonists, p38 MAPK inhibitors, and microglia regulators like cromolyn and furosemide have shown potential in reducing neuroinflammation and improving cognitive function. Chinese herbal polysaccharides, such as those from *Ganoderma lucidum* and *Astragalus*, also exhibit anti-neuroinflammatory and neuroprotective effects. Despite the progress, challenges remain in developing effective treatments for AD. The complex interactions between microglia and AD pathology, along with the need for long-term clinical trials, highlight the ongoing research efforts to understand and treat this debilitating disease.Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized by progressive memory and cognitive decline. The pathogenesis of AD involves the accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles (NFTs), primarily due to the hyperphosphorylation of tau protein. Microglial activation, a key component of neuroinflammation, plays a crucial role in AD by enhancing Aβ clearance and driving the spread of tau proteins. This review explores the connection between microglial energy metabolic disorders, neuroinflammation, and AD development, highlighting the potential of anti-inflammatory and microglia-regulating therapies. Microglia, the primary immune cells in the central nervous system (CNS), are involved in various physiological processes such as brain development, activity, and plasticity. They can polarize into anti-inflammatory 'M2' or pro-inflammatory 'M1' phenotypes, with the latter being associated with neuronal damage and degeneration. Chronic microglial activation leads to a vicious cycle of Aβ and tau accumulation, contributing to neurodegeneration and cognitive decline. The energy metabolic disorders of microglia, particularly the switch from oxidative phosphorylation (OXPHOS) to glycolysis, are critical in driving neuroinflammation. Pro-inflammatory cytokines and other mediators produced during glycolysis further exacerbate neuroinflammation and neuronal damage. Targeting glycolytic pathways and microglial polarization may provide new therapeutic approaches to mitigate neuroinflammation and its harmful effects. Recent advancements in anti-inflammatory drugs and microglia regulators offer promising strategies for AD treatment. Non-steroidal anti-inflammatory drugs (NSAIDs), TLR4 antagonists, p38 MAPK inhibitors, and microglia regulators like cromolyn and furosemide have shown potential in reducing neuroinflammation and improving cognitive function. Chinese herbal polysaccharides, such as those from *Ganoderma lucidum* and *Astragalus*, also exhibit anti-neuroinflammatory and neuroprotective effects. Despite the progress, challenges remain in developing effective treatments for AD. The complex interactions between microglia and AD pathology, along with the need for long-term clinical trials, highlight the ongoing research efforts to understand and treat this debilitating disease.