Neuronal loss of NCLX-dependent mitochondrial calcium efflux mediates age-associated cognitive decline.

ABSTRACT: Mitochondrial calcium overload contributes to neurodegenerative disease development and progression. We recently reported that loss of the mitochondrial sodium/calcium exchanger (NCLX), the primary mechanism of _mCa²⁺ efflux, promotes _mCa²⁺ overload, metabolic derangement, redox stress, and cognitive decline in models of Alzheimer's disease (AD). However, whether disrupted _mCa²⁺ signaling contributes to neuronal pathology and cognitive decline independent of pre-existing amyloid or tau pathology remains unknown. Here, we generated mice with neuronal deletion of the mitochondrial sodium/calcium exchanger (NCLX, Slc8b1 gene), and evaluated age-associated changes in cognitive function and neuropathology. Neuronal loss of

SUBMITTER: Jadiya P 

PROVIDER: S-EPMC10014305 | biostudies-literature | 2023 Mar

REPOSITORIES: biostudies-literature