Abstract
BackgroundSchizophrenia is currently considered to be a polygene-related disease with unknown etiology. This research will verify whether the single nucleotide polymorphism (SNP) of the long intergenic noncoding RNA01080 (linc01080) contributes to the susceptibility and phenotypic heterogeneity of schizophrenia, with a view to providing data support for the prevention and individualized treatment of this disease.MethodThe SNP rs7990916 in linc01080 were genotyped in 1139 schizophrenic and 1039 controls in a Southern Chinese Han population by the improved multiplex ligation detection reaction (imLDR) technique. Meanwhile, we assessed and analyzed the association between this SNP and schizophrenics’ clinical symptoms, and the cognitive function.ResultThere was no significant difference in genotype distribution, allele frequency distribution, gender stratification analysis between the two groups. However, the SNP of rs7990916 was significantly associated with the age of onset in patients with schizophrenia (P = 8.22E-07), patients with T allele had earlier onset age compared with CC genotype carriers. In terms of cognitive function, patients with T allele scored lower than CC genotype carriers in the Tower of London score and symbol coding score in the Brief assessment of Cognition (BACS), and the difference was statistically significant (P = 0.014, P = 0.022, respectively).ConclusionOur data show for the first time that linc01080 polymorphism may affect the age of onset and neurocognitive function in patients with schizophrenia.
Highlights
Schizophrenia is currently considered to be a polygene-related disease with unknown etiology
Our data show for the first time that linc01080 polymorphism may affect the age of onset and neurocognitive function in patients with schizophrenia
Schizophrenia is a disease with different heterogeneity in clinical symptoms, onset age, cognitive function and brain structure [1], which was once regarded as basing on abnormal neurodevelopment
Summary
Schizophrenia is currently considered to be a polygene-related disease with unknown etiology. LincRNA1230 can limit the junction of WD repeat 5 to the promoter region of neural lineage related genes, it could prevent the transformation of mouse neural stem cells into neural progenitor cells [8], LncRNAlinc00115 regulates the self-renewal and proliferation of neural stem cells by activating transforming growth factor-β and linc00152 through activating miR-103a-3p / FEZF axis [9, 10], Linc01198 promotes glioma proliferation by enhancing NEDD4–1-dependent PTEN inhibition [11] This proliferation and differentiation function of NSCs is obviously related to brain homeostasis, and may even change in mental and nervous system diseases [12]
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