Cell type-specific mitochondrial dysfunction in AD pathogenesis. Many mitochondria are located in nerve terminals, contributing to supply energy for the production of neurotransmitters and the transport and release of synaptic vesicles. The damage of synaptic mitochondria causes abnormal synaptic activity in AD. Astrocyte regulates neuronal activity by buffering excess neurotransmitters at synapses through its mitochondria and metabolism. When astrocytic mitochondria are disrupted, neuronal hyperactivity may be triggered in AD. Also, since the β-oxidation process in astrocytic mitochondria exclusively consumes toxic fatty acids or lipid particles, astrocytic mitochondria play crucial roles in the removal of lipid particles associated with APOE in AD. The inflammatory status of microglia is determined by mitochondria and metabolic signaling in response to external stimuli. AD pathology cause metabolic reprogramming in microglia with the inflammatory response to become the activated or tolerance status.