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- W3192254541 abstract "Alzheimer's disease (AD) is the most common progressive neurodegenerative disease. However, the underlying molecular mechanism is incompletely understood. Here we report that the pro-apoptotic protein BAD as a key regulator for neuronal apoptosis, neuroinflammation and Aβ clearance in AD. BAD pro-apoptotic activity is significantly increased in neurons of AD patients and 5XFAD mice. Conversely, genetic disruption of Bad alleles restores spatial learning and memory deficits in 5XFAD mice. Mechanistically, phosphorylation and inactivation of BAD by neurotropic factor-activated Akt is abrogated in neurons under AD condition. Through reactive oxygen species (ROS)-oxidized mitochondrial DNA (mtDNA) axis, BAD also promotes microglial NLRP3 inflammasome activation, thereby skewing microglia toward neuroinflammatory microglia to inhibit microglial phagocytosis of Aβ in AD mice. Our results support a model in which BAD contributes to AD pathologies by driving neuronal apoptosis and neuroinflammation but suppressing microglial phagocytosis of Aβ, suggesting that BAD is a potential therapeutic target for AD." @default.
- W3192254541 created "2021-08-16" @default.
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- W3192254541 date "2021-09-01" @default.
- W3192254541 modified "2023-10-14" @default.
- W3192254541 title "BAD-mediated neuronal apoptosis and neuroinflammation contribute to Alzheimer's disease pathology" @default.
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- W3192254541 doi "https://doi.org/10.1016/j.isci.2021.102942" @default.
- W3192254541 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8369003" @default.
- W3192254541 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34430820" @default.