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Obsessive–compulsive disorder (OCD) presents several diagnostic and treatment challenges, in part because etiology and pathogenesis remains relatively unknown. Most studies of OCD focus on adult patients, but there have been some studies of OCD onset before the age of 6 years, and the vast majority of OCD patients (80%) report that related symptoms began before age 18.
Obsessive—compulsive disorder (OCD) presents several diagnostic and treatment challenges, in part because etiology and pathogenesis remains relatively unknown. Most studies of OCD focus on adult patients, but there have been some studies of OCD onset before the age of 6 years, and the vast majority of OCD patients (80%) report that related symptoms began before age 18.
Although it is well-accepted that OCD is caused by both genetic and environmental factors, identifying those factors has proven elusive. Molecular genetic studies of OCD have usually focused on the monoamine pathway genes and have zoned in on several receptors thought to play a key role in the development of the condition, including catechol O-methyltransferase gene, the serotonin 2β receptor (5HT2B) gene, and the serotonin transporter gene, among others.
A new study in Neuropsychiatric Disease and Treatment analyzed the role of micro-ribonucleic acids (miRNAs)—small noncoding RNAs that regulate approximately 30% of human protein coding gene expression at the post-transcriptional level—in the incidence and severity of OCD in children. This area of study is complicated by the fact that linking psychiatric disorders to specific causative genes has proven elusive, at best. “The involvement of multiple signaling pathways in psychiatric disease complicates both the investigation of the underlying biological causes and efforts to identify effective therapies,” the researchers note.
The study examined miR18a-5p, miR22-3p, miR24-3p, miR106b-5p, miR107, miR125b-5p, and miR155a-5p levels in children and adolescents (ranging in age from 7-17 years) with OCD, based in part on previous research indicating their role in the etiology of OCD. miR22k, for example, has been associated with panic disorder and anxiety. “We think that DNA damage, oxidative stress, hypoxia, and inflammation-related molecular mechanisms may be dysregulated in OCD,” the study authors note.
The small sample consisted of 23 patients from Harran University Faculty of Medicine Research Hospital, Child and Adolescent Psychiatry Clinic, who were diagnosed with OCD, and 40 healthy volunteer controls. The researchers found significantly increased levels of miR22-3p, miR24-3p, miR106b-5p, miR125b-5p, and miR155a-5p levels in OCD patients compared with controls.There were no statistically significant differences in miR18a-5p or miR107 levels between groups (P≥0.05).
The researchers note that their study had some limitations, including the small sample size and the limited number of miRNA types analyzed, along with the fact that a paucity of previous research in this area limits the ability to compare the findings with previous studies. But these results, although preliminary, should encourage further research into the how the dysregulation of circulating miRNA impacts psychiatric disorders in OCD and beyond.