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2 results

  • Effect of DISC1 Polymorphisms on the Long-term Course of Neurocognitive Deficits in Non-affective Psychosis

  • J. Vázquez-Bourgon, R. Ayesa-Arriola, M. Fatjó-Vilas, R. Roiz-Santiañez, L. Fañanás, B. Crespo-Facorro
  • Journal:
    European Psychiatry / Volume 30 / Issue 7 / October 2015
    Published online by Cambridge University Press:
    16 April 2020, pp. 861-867

  • Neurocognitive deficits are core symptoms of schizophrenia that determine a poorer outcome. High variability in the progression of neuropsychological deficits in schizophrenia has been described. It is still unknown whether genetic variations can affect the course of cognitive deficits. Variations in the Disrupted in Schizophrenia 1 (DISC1) gene have previously been associated with neurocognitive deficits. This study investigated the association between 3 DISC1 polymorphisms (rs6675281 (Leu607Phe), rs1000731, and rs821616 (Ser704Cys)) and long-term (3 years) cognitive performance. One-hundred-thirty-three Caucasian drug-naive patients experiencing a first episode of non-affective psychosis were genotyped. Cognitive function was assessed at baseline and after 3 years of initiating treatment. Other clinical and socio-demographic variables were recorded to eliminate potential confounding effects. Patients carrying the A allele of rs1000731 exhibited a significant improvement in Working Memory and Attention domains, and the homozygosity of the A allele of rs821616 showed a significant improvement in Motor Dexterity performance over 3 years of follow-up. In conclusion, DISC1 gene variations may affect the course of cognitive deficits found in patients suffering from the first episode of non-affective psychosis.

  • Catecholaminergic neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia

  • Shuji Iritani, Hirotaka Sekiguchi, Chikako Habuchi, Youta Torii, Keisuke Kuroda, Kozo Kaibuchi, Norio Ozaki
  • Journal:
    Acta Neuropsychiatrica / Volume 28 / Issue 2 / April 2016
    Published online by Cambridge University Press:
    03 September 2015, pp. 117-123
  • Background

    The precise aetiology of schizophrenia remains unclear. The neurodevelopmental hypothesis of schizophrenia has been proposed based on the accumulation of genomic or neuroimaging studies.

    Objective

    In this study, we examined the catecholaminergic neuronal networks in the frontal cortices of disrupted-in-schizophrenia 1 (DISC1) knockout (KO) mice, which are considered to be a useful model of schizophrenia.

    Methods

    Six DISC1 homozygous KO mice and six age-matched littermates were used. The animals’ brains were cut into 20-μm-thick slices, which were then immunohistochemically stained using an anti-tyrosine hydroxylase (TH) monoclonal antibody.

    Results

    The TH-immunopositive fibres detected in the orbitofrontal cortices of the DISC1 KO mice were significantly shorter than those seen in the wild-type mice.

    Conclusion

    These neuropathological findings indicate that the hypofrontal symptoms of schizophrenia are associated with higher mental function deficiencies or cognitive dysfunction such as a loss of working memory.