Published Paper Details:

A serious psychiatric condition called obsessive-compulsive disorder (OCD) affects about 2% of both children and adults in society. OCD has been linked to families in studies of family aggregation, and findings from twin studies show that this relationship is partially influenced by genetic factors. Only three genome-wide linkage studies have been finished so far, and the findings are merely suggestive. More than 80 candidate gene studies have also been released. These studies have mainly concentrated on genes in the dopaminergic and serotonergic pathways. Unfortunately, none have been replicated and, with the exception of the glutamate transporter gene, none have reached genome-wide significance. In order to obtain sufficiently large samples of people with OCD, use cutting-edge laboratory techniques, and carry out the bioinformatic analyses necessary to identify risk loci, multidisciplinary teams of investigators will need to collaborate in future studies. Steroids may be influencing how the disorder develops, according to some theories. However, only a few studies have examined hormone levels and obsessive-compulsive (OC) symptoms simultaneously to date; as a result, there is little direct proof of this association. As a result, more thorough research into neurotransmission in OC patients has linked OCD pathology to the serotonergic, dopaminergic, and glutamatergic neurotransmitter systems. The molecular and cellular mechanisms underlying the pathogenesis of "obsessive-compulsive disorder-like" behaviors have started to come into focus in recent studies of novel mouse genetic models with excessive grooming behaviors Hoxb8, Sapap3, and Slitrk5 are three genes that are genetically deleted in mice, resulting in pathological behaviors such as adult-onset excessive grooming with mild to severe hair loss and self-injury. The abnormal grooming behaviors are linked to increased anxiety in two of the models, the Sapap3-deficient and the Slitrk5-deficient mice, and these pathological behaviors can be reduced with subchronic administration of a selective serotonin reuptake inhibitor, indicating the predictive validity of such models. These models' molecular, pathophysiological, and genetic analyses offer several new insights into the causes of these mice's abnormal behaviors. In this review, we are going to focus on understanding these genetic and hormonal influences in triggering OCD.