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A decrease in protein level and a missense polymorphism of KIF17 are associated with schizophrenia.

Woraphat Ratta-Apha1, Kentaro Mouri1, Shuken Boku1

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Kinesin superfamily motor protein 17 (KIF17) levels are lower in schizophrenia brains, suggesting its dysfunction may contribute to the disease. Genetic variants in KIF17 were initially linked to schizophrenia but not consistently replicated.

Keywords:
KIF17Postmortem brainSchizophreniaSingle nucleotide polymorphism

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Area of Science:

  • Neuroscience
  • Genetics
  • Psychiatry

Background:

  • N-methyl-D-aspartate (NMDA) receptor dysfunction is implicated in schizophrenia pathophysiology.
  • The GluN2B subunit of NMDA receptors and its trafficking complex are altered in schizophrenia's prefrontal cortex.
  • Kinesin superfamily motor protein 17 (KIF17) transports the NR2B subunit and its gene variants have been associated with schizophrenia.

Purpose of the Study:

  • To investigate KIF17 protein levels in postmortem prefrontal cortex of schizophrenia patients.
  • To examine the association of KIF17 missense polymorphisms with schizophrenia.
  • To explore the role of KIF17 dysfunction in schizophrenia.

Main Methods:

  • Quantification of KIF17 protein expression in postmortem brain tissue from schizophrenia patients and controls.
  • Genotyping analysis of KIF17 missense polymorphisms (rs631375, rs13375609, rs522496, rs2296225) in large cohorts of schizophrenia patients and healthy subjects.
  • Replication study with independent cohorts and analysis of KIF17 mRNA expression based on rs2296225 alleles.

Main Results:

  • Significantly lower KIF17 protein expression was observed in the prefrontal cortex of schizophrenia patients compared to controls.
  • The rs2296225 polymorphism in KIF17 showed significant differences in genotypic distribution and allelic frequency in initial chronic schizophrenia cohorts.
  • These findings for rs2296225 were not replicated in independent cohorts, and its alleles did not affect KIF17 mRNA expression.

Conclusions:

  • KIF17 protein levels are reduced in the prefrontal cortex of individuals with schizophrenia.
  • While initial genetic association studies suggested a link between KIF17 variants and schizophrenia, these findings lacked replication and functional evidence.
  • The results suggest that KIF17 dysfunction, potentially independent of the studied genetic variants, may be involved in the pathophysiology of schizophrenia.