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Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within...

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

Ya-Qi Zhang^1,2,3, Xin Cai^1,2, Qing Zhang^4,5

¹State Key Laboratory of Genetic Evolution & Animal Models, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650201, China.

Schizophrenia Bulletin

|May 23, 2025

Summary

Akap11 deficiency in mice causes synaptic and behavioral deficits relevant to schizophrenia. This research highlights AKAP11 as a significant risk gene for schizophrenia, implicating synaptic dysfunction in its pathogenesis.

Keywords:

AKAP11 Dendritic spines Synapses anxiety-like behaviors prepulse inhibition schizophrenia

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Last Updated: Jan 18, 2026

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Area of Science:

Neuroscience
Genetics
Molecular Biology

Background:

Rare protein-truncating variants (PTVs) in AKAP11 are linked to schizophrenia risk.
Previous studies noted EEG and synaptic proteome alterations in Akap11 mutant mice.
Synaptic dysfunction is hypothesized to contribute to AKAP11 deficiency in schizophrenia pathogenesis.

Purpose of the Study:

To investigate the impact of Akap11 deficiency on schizophrenia-relevant phenotypes.
To elucidate the role of Akap11 in synaptic function and behavior.

Main Methods:

Generated Akap11 knockout mice for study.
Conducted behavioral evaluations, neuronal sparse labeling, and electron microscopy.
Utilized immunoprecipitation mass spectrometry (IP-MS) to identify Akap11 interaction proteins.

Main Results:

Akap11 deficient mice showed impaired prepulse inhibition and anxiety-like behaviors.
Reduced spine density and altered synaptogenesis (synapses, vesicles, PSD length) were observed.
Identified 222 Akap11 interacting proteins, including synaptic and actin-related proteins, suggesting roles in RNA splicing, cell organization, and signaling pathways.

Conclusions:

Akap11 deficiency leads to synaptic and behavioral deficits in mice.
These findings support AKAP11's significance as a schizophrenia risk gene.
The study provides insights into the mechanisms linking AKAP11 to schizophrenia pathogenesis.