Schizophrenia is a destructive neuropsychiatric disease with a median prevalence of 4.0 per 1,000 during the whole life. Genome-wide association studies have shown the role of copy number variants (generally deletions) and certain alleles of common single nucleotide polymorphisms in the pathogenesis of
schizophrenia. This disorder predominantly follows the polygenic inheritance model.
Schizophrenia has also been linked with various alterations in the transcript and
protein content of the brain tissue. Recent studies indicate that alterations in non-coding RNAs (ncRNAs) signature underlie a proportion of this dysregulation. High throughput microarray investigations have demonstrated momentous alterations in the expression of long non-coding RNAs (
lncRNA) and
microRNAs (
miRNAs) in the circulation or post-mortem brain tissues of patients with
schizophrenia compared with control samples. While Gomafu, PINT, GAS5, TCONS_l2_00021339, IFNG-AS1, FAS-AS1, PVT1, and TUG1 are among down-regulated lncRNAs in
schizophrenia, MEG3, THRIL, HOXA-AS2, Linc-ROR, SPRY4-IT1, UCA1, and MALAT1 have been up-regulated in these patients. Moreover, several
miRNAs, such as miR-30e, miR-130b, hsa-miR-130b, miR-193a-3p, hsa-miR-193a-3p,
hsa-miR-181b, hsa-miR-34a,
hsa-miR-346, and
hsa-miR-7 have been shown to be dysregulated in blood or brain samples of patients with
schizophrenia. Dysregulation of these transcripts in
schizophrenia not only provides insight into the pathogenic processes of this disorder, it also suggests these transcripts could serve as diagnostic markers for
schizophrenia. In the present paper, we explore the changes in the expression of
miRNAs and lncRNAs in patients with
schizophrenia.