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Mitochondrial dysfunction in oxidative phosphorylation (OXPHOS) is linked to schizophrenia (SCZ). This review highlights OXPHOS abnormalities at the functional level, suggesting new therapeutic targets for this complex brain disorder.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Genetics

Background:

  • Schizophrenia (SCZ) is a severe mental disorder with unknown causes and limited treatments.
  • Early-life bioenergetic deficits in oxidative phosphorylation (OXPHOS) may disrupt brain development and function in SCZ.
  • Mitochondrial dysfunction is increasingly implicated in SCZ pathophysiology.

Purpose of the Study:

  • To review current evidence linking mitochondrial OXPHOS dysfunction to SCZ.
  • To focus on enzymatic and functional alterations in OXPHOS, rather than genetic or oxidative stress markers.
  • To explore the role of OXPHOS dysfunction in SCZ pathogenesis and potential therapeutic strategies.

Main Methods:

  • This is a narrative review of existing literature.
  • Focus on studies examining OXPHOS function at the enzymatic/functional level in SCZ.
  • Inclusion of evidence from both central and peripheral tissues.

Main Results:

  • Evidence links OXPHOS dysfunction, including alterations in multiple complexes, to SCZ.
  • OXPHOS impairment affects broader mitochondrial function and is associated with oxidative stress.
  • Dysfunctional OXPHOS contributes to SCZ through apoptosis, aging, and synaptic deterioration.

Conclusions:

  • Mitochondrial OXPHOS abnormalities are a significant biological feature of SCZ.
  • OXPHOS dysfunction may be both a cause and consequence of SCZ, impacting disease progression.
  • Targeting OXPHOS dysregulation offers potential for novel SCZ therapies.