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Mitochondrial Dysfunction in Schizophrenia.

Peiyan Ni1, Sangmi Chung2

  • 1Psychiatric Laboratory and Mental Health Center, The State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, 610041, China.

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology
|April 28, 2020
PubMed
Summary
This summary is machine-generated.

Mitochondrial dysfunction is increasingly linked to schizophrenia (SCZ), a neurodevelopmental disorder. Targeting these cellular energy problems may lead to new treatments for SCZ symptoms unresponsive to current medications.

Keywords:
developmentmitochondrianeuronsschizophreniatherapeutic targets

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Psychiatry

Background:

  • Schizophrenia (SCZ) is a severe neurodevelopmental disorder with significant global health and economic impacts.
  • Current antipsychotics primarily treat positive symptoms, leaving negative and cognitive symptoms inadequately addressed.
  • Understanding SCZ pathogenesis is crucial for developing improved therapeutic strategies.

Purpose of the Study:

  • To critically review recent evidence linking mitochondrial dysfunction to SCZ pathogenesis.
  • To explore the potential of targeting mitochondrial function for novel SCZ treatments.

Main Methods:

  • Literature review of postmortem, imaging, genetic, and induced pluripotent stem cell studies in SCZ.
  • Analysis of animal models exhibiting mitochondrial dysfunction and SCZ-relevant behaviors.

Main Results:

  • Consistent evidence indicates compromised mitochondrial function in individuals with SCZ.
  • Animal models demonstrate that mitochondrial dysfunction can induce SCZ-like neurobehavioral abnormalities.
  • Restoration of mitochondrial function emerges as a promising therapeutic avenue.

Conclusions:

  • Mitochondrial dysfunction is a significant factor in SCZ pathogenesis.
  • Targeting mitochondrial pathways offers a novel therapeutic strategy for SCZ, potentially addressing unmet clinical needs.