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Reduced protein synthesis in schizophrenia patient-derived olfactory cells

J A English1, Y Fan2, M Föcking1

  • 1Department of Psychiatry, University College of Dublin School of Biomolecular & Biomedical Science, Royal College of Surgeons in Ireland, Dublin, Ireland.

Translational Psychiatry
|October 21, 2015
PubMed

Insights

Schizophrenia is linked to reduced protein synthesis in brain cells, specifically olfactory neurosphere-derived (ONS) cells. This discovery highlights cell-type specific deficits and implicates key translational control pathways in the disorder.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Schizophrenia pathogenesis remains incompletely understood at the cellular level.
  • Olfactory neurosphere-derived (ONS) cells offer a model for studying neuronal pathology in schizophrenia.
  • Previous research has not fully elucidated the role of protein synthesis in schizophrenia.

Purpose of the Study:

  • To investigate cellular pathology in schizophrenia using human ONS cells.
  • To identify molecular mechanisms underlying schizophrenia, focusing on protein synthesis.
  • To integrate proteomic, transcriptomic, and genomic data to understand schizophrenia pathophysiology.

Main Methods:

  • Discovery-based proteomics and targeted functional analyses on ONS cells from schizophrenia patients and controls.
  • Quantification of global protein synthesis rates in vitro.
  • Pathway analysis of proteomic and transcriptomic data, integrated with genome-wide association study (GWAS) data.

Main Results:

  • Reduced ribosomal protein levels and overall ribosomal signal intensity in schizophrenia patient-derived ONS cells.
  • Significantly decreased global protein synthesis rates in ONS cells from schizophrenia patients compared to controls.
  • Cell type-specific effects observed, as fibroblast protein synthesis rates did not differ.
  • Perturbation of eIF2α, eIF4, and mammalian target of rapamycin (mTOR) translational control pathways identified.
  • Genomic analysis implicated EIF2AK2 and confirmed the role of these translational pathways.

Conclusions:

  • Dysregulated protein synthesis is implicated in schizophrenia for the first time.
  • Cell type-specific deficits in protein synthesis contribute to schizophrenia pathophysiology.
  • Translational control pathways (eIF2α, eIF4, mTOR) are critical in schizophrenia, supported by proteomic, transcriptomic, and genomic data.

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