The interaction between microglial dysfunction and mitochondrial impairment in Alzheimer’s disease

Alzheimer's disease (AD), a prevalent form of dementia in the elderly, is characterized by marked neurodegeneration and cognitive decline. Central to its pathology are Amyloid-beta plaques, neurofibrillary tangles, and neuroinflammation. This review delves into the pivotal role of microglia, the primary immune cells in the central nervous system, in AD's progression. We highlight recent discoveries revealing how abnormal microglial activity, influenced by mitochondrial dysfunction, contributes to AD development. Special attention is given to the bidirectional relationship between microglia and mitochondria, including the impact of metabolic disturbances and energy dysregulation on microglial function. Further, we explore the mechanisms underlying microglial activation and its consequences on neuronal health, including the interplay between inflammatory pathways and mitochondrial dynamics. Our comprehensive analysis underscores the significance of mitochondrial homeostasis in microglial functionality and its implications for AD progression, offering insights into potential therapeutic avenues targeting microglial mitochondria in AD.