Schizophrenia-Related Synaptic Dysfunction and Abnormal Sensorimotor Gating in Akap11-Deficient Mice.

ABSTRACT:

Background and hypothesis

Large-scale whole exome sequencing (WES) analyses have implicated rare protein-truncating variants (PTVs) in the AKAP11 gene contributing to schizophrenia risk. Previous studies reported alterations of EEG characteristics and synaptic proteome in Akap11 mutant mice. We hypothesize that synaptic dysfunction contributes to AKAP11 deficiency in the pathogenesis of schizophrenia.

Study design

We generated an Akap11 knockout mouse and employed a series of behavioral evaluations, neuronal sparse labeling assays, electron microscopy, and immunoprecipitation mass spectrometry (IP-MS) to elucidate the impacts of Akap11 on schizophrenia-relevant phenotypes.

Study results

Our behavioral paradigm evaluations revealed that Akap11 deficient mice exhibited

SUBMITTER: Zhang YQ 

PROVIDER: S-EPMC12809822 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature