1208-Epigenetic Control of Microglial Immunity in Alzheimer

Recent research identifies the histone acetyltransferase KAT7 as a primary epigenetic driver of chronic neuroinflammation in Alzheimer’s disease. By increasing H3K14 acetylation at the Cmpk2 promoter, KAT7 triggers the synthesis and cytosolic release of mitochondrial DNA (mtDNA) in microglia. This leakage activates the cGAS-STING and NLRP3 immune pathways, which fuel a persistent inflammatory cycle that worsens the disease. Experiments in 5×FAD mouse models demonstrate that removing or chemically inhibiting KAT7 reduces amyloid-beta accumulation and lowers neuroinflammation. Furthermore, targeting this epigenetic axis successfully restores synaptic plasticity and enhances cognitive performance. These findings establish KAT7 as a promising therapeutic target for mitigating the progression of dementia and related neurological disorders.References:Liu Y, Ye Y, Fan M, et al. Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer’s disease pathogenesis[J]. Neuron, 2026.前往小宇宙评论区与主播互动