Pathogenesis Of Obsessive-compulsive Disorder Research Articles

Inflammation in obsessive-compulsive disorder: A literature review and hypothesis-based potential of transcranial photobiomodulation.

Obsessive-compulsive disorder (OCD) is a disabling neuropsychiatric disorder that affects about 2%-3% of the global population. Despite the availability of several treatments, many patients with OCD do not respond adequately, highlighting the need for new therapeutic approaches. Recent studies have associated various inflammatory processes with the pathogenesis of OCD, including alterations in peripheral immune cells, alterations in cytokine levels, and neuroinflammation. These findings suggest that inflammation could be a promising target for intervention. Transcranial photobiomodulation (t-PBM) with near-infrared light is a noninvasive neuromodulation technique that has shown potential for several neuropsychiatric disorders. However, its efficacy in OCD remains to be fully explored. This study aimed to review the literature on inflammation in OCD, detailing associations with T-cell populations, monocytes, NLRP3 inflammasome components, microglial activation, and elevated proinflammatory cytokines such as TNF-α, CRP, IL-1β, and IL-6. We also examined the hypothesis-based potential of t-PBM in targeting these inflammatory pathways of OCD, focusing on mechanisms such as modulation of oxidative stress, regulation of immune cell function, reduction of proinflammatory cytokine levels, deactivation of neurotoxic microglia, and upregulation of BDNF gene expression. Our review suggests that t-PBM could be a promising, noninvasive intervention for OCD, with the potential to modulate underlying inflammatory processes. Future research should focus on randomized clinical trials to assess t-PBM's efficacy and optimal treatment parameters in OCD. Biomarker analyses and neuroimaging studies will be important in understanding the relationship between inflammatory modulation and OCD symptom improvement following t-PBM sessions.

Human microbiota from drug-naive patients with obsessive-compulsive disorder drives behavioral symptoms and neuroinflammation via succinic acid in mice.

Emerging evidence suggests that the gut microbiota is closely related to psychiatric disorders. However, little is known about the role of the gut microbiota in the development of obsessive-compulsive disorder (OCD). Here, to investigate the contribution of gut microbiota to the pathogenesis of OCD, we transplanted fecal microbiota from first-episode, drug-naive OCD patients or demographically matched healthy individuals into antibiotic-treated specific pathogen-free (SPF) mice and showed that colonization with OCD microbiota is sufficient to induce core behavioral deficits, including abnormal anxiety-like and compulsive-like behaviors. The fecal microbiota was analyzed using 16 S rRNA full-length sequencing, and the results demonstrated a clear separation of the fecal microbiota of mice colonized with OCD and control microbiota. Notably, microbiota from OCD-colonized mice resulted in injured neuronal morphology and function in the mPFC, with inflammation in the mPFC and colon. Unbiased metabolomic analyses of the serum and mPFC region revealed the accumulation of succinic acid (SA) in OCD-colonized mice. SA impeded neuronal activity and induced an inflammatory response in both the colon and mPFC, impacting intestinal permeability and brain function, which act as vital signal mediators in gut microbiota-brain-immune crosstalk. Manipulations of dimethyl malonate (DM) have been reported to exert neuroprotective effects by suppressing the oxidation of accumulated succinic acid, attenuating the downstream inflammatory response and neuronal damage, and can help to partly improve abnormal behavior and reduce neuroinflammation and intestinal inflammation in OCD-colonized mice. We propose that the gut microbiota likely regulates brain function and behaviors in mice via succinic acid signaling, which contributes to the pathophysiology of OCD through gut-brain crosstalk and may provide new insights into the treatment of this disorder.

Baclofen and 4-Phenylpyrrolidone Derivative GIZH-290 Attenuates Compulsive-Like Behavior in Mice

Obsessive-compulsive disorder (OCD) is a mental disease characterized by the obsessions which cause marked distress or anxiety and/or compulsions intended to alleviate this distress. The results of experimental and clinical studies suggest a possible role of GABAB receptors in the pathogenesis of OCD, making it relevant to study the effect of ligands of these receptors on the behavior of rodents. Objectives: Studying the effects of GIZH-290 and baclofen in animal models of OCD. Methods. The effects of GIZH-290 (0.01, 0.1, 1 mg/kg, i.p.) and baclofen (0.1, 1, and 5 mg/kg, i.p.) were studied in the marble burying test and the rotarod test, as well as in the 8-OH-DPAT-induced decrease in spontaneous alternation in mice. Results. Baclofen and GIZH-290 attenuated compulsive-like behavior in mice by reducing the number of buried marbles in the marble burying test at all tested doses. However, the effect of baclofen at a dose of 5 mg/kg was accompanied by a disruption of the animals’ motor coordination in the rotarod test. At the same time, neither baclofen nor GIZH-290 attenuated 8-OH-DPAT-induced (2 mg/kg, i.p.) decrease in spontaneous alternation behavior in mice. On the contrary, baclofen at a dose of 1 mg/kg exacerbated this disruption. Conclusion. Baclofen and GIZH-290 have anticompulsive activity in the marble burying test, but not in the 8-OH-DPAT-induced decrease in spontaneous alternation behavior in mice.

Association of cortical gyrification, white matter microstructure, and phenotypic profile in medication-naïve obsessive-compulsive disorder.

Obsessive-compulsive disorder (OCD) is thought to arise from dysconnectivity among interlinked brain regions resulting in a wide spectrum of clinical manifestations. Cortical gyrification, a key morphological feature of human cerebral cortex, has been considered associated with developmental connectivity in early life. Monitoring cortical gyrification alterations may provide new insights into the developmental pathogenesis of OCD. Sixty-two medication-naive patients with OCD and 59 healthy controls (HCs) were included in this study. Local gyrification index (LGI) was extracted from T1-weighted MRI data to identify the gyrification changes in OCD. Total distortion (splay, bend, or twist of fibers) was calculated using diffusion-weighted MRI data to examine the changes in white matter microstructure in patients with OCD. Compared with HCs, patients with OCD showed significantly increased LGI in bilateral medial frontal gyrus and the right precuneus, where the mean LGI was positively correlated with anxiety score. Patients with OCD also showed significantly decreased total distortion in the body, genu, and splenium of the corpus callosum (CC), where the average distortion was negatively correlated with anxiety scores. Intriguingly, the mean LGI of the affected cortical regions was significantly correlated with the mean distortion of the affected white matter tracts in patients with OCD. We demonstrated associations among increased LGI, aberrant white matter geometry, and higher anxiety in patients with OCD. Our findings indicate that developmental dysconnectivity-driven alterations in cortical folding are one of the neural substrates underlying the clinical manifestations of OCD.

Gender differences in the symptoms and physiological basis of Obsessive-Compulsive Disorder

Obsessive-compulsive disorder (OCD) is an anxiety disorder related to repetitive behaviors and intrusive thoughts. Individuals with OCD experience conscious, self-imposed compulsions and counter-compulsions, which result in high levels of anxiety and difficulties in social interactions. OCD is a common mental disorder with onset often in adolescence. Gender differences in OCD exist, with males reporting earlier symptom onset, and females experiencing symptoms during adolescence, pregnancy, or postpartum, particularly related to contamination and/or aggressive obsessions. Neurobiological factors play a role in OCD etiology. Genetic studies show hereditary tendencies, with gender differences observed. Brain structure research identifies differences between male and female patients. Dopamine and plasma norepinephrine are implicated in OCD pathogenesis. Understanding gender differences is crucial for OCD diagnosis and treatment. Further research is needed to validate and explain these differences in order to inform advancements in OCD treatment approaches. This paper summarizes and discusses the relationship between OCD and gender, focusing on epidemiological characteristics, symptoms, and physiological basis of OCD, emphasizing gender differences. Future research directions in the field of OCD are presented.

Sex-dependent association of DNA methylation of HPA axis-related gene FKBP5 with obsessive-compulsive disorder

AimsAlthough hypothalamic-pituitary-adrenal (HPA) axis dysregulation in obsessive-compulsive disorder (OCD) has been reported, epigenetic changes in HPA axis-related genes have not been well studied in OCD. The present study investigated whether the epigenetic regulation of FK506-binding protein 51 gene (FKBP5) intron 7 is associated with OCD status in each sex. In addition, relationships among the DNA methylation levels of FKBP5 intron 7, OCD status and early-life trauma were explored. MethodsA total of 267 patients with OCD and 201 controls aged between 18 and 40 years were recruited. Demographic and clinical assessment, FKBP5 rs1360780 genotyping, and pyrosequencing of FKBP5 intron 7 were conducted. DNA was extracted from peripheral blood leucocytes. First, multivariate analysis of covariance for differential DNA methylation levels between OCD patients and controls was conducted with adjustment for FKBP5 rs1360780 genotype, early-life trauma, depressive symptoms, and age as covariates in each sex. Next, path analysis was conducted to determine the mediation effects of DNA methylation levels of FKBP5 between early-life trauma and OCD status. In addition, sensitivity analyses for medication and lifetime major depression were also performed. ResultsDNA methylation at the FKBP5 intron 7 CpG site was significantly lower in men with OCD, compared to controls (mean difference −1.33%, 95% CI −2.11 to −0.55, p < 0.001). The results remained significant for drug naïve or free subjects (mean difference −1.27%, 95% CI −2.18 to −0.37, p = 0.006, in men) and for subjects without lifetime major depressive disorder (mean difference −1.60%, 95% CI −2.54 to −0.66, p < 0.001, in men). The mediation effect of DNA methylation levels was not significant between early-life trauma and OCD status. ConclusionThese findings suggest that epigenetic factors of HPA axis-related gene FKBP5 may play a role in the pathogenesis of OCD. Further studies are needed to determine how altered DNA methylation of FKBP5 intron 7 and HPA axis function are involved in OCD.

Epigenome-wide analysis identifies methylome profiles linked to obsessive-compulsive disorder, disease severity, and treatment response.

Obsessive-compulsive disorder (OCD) is a prevalent mental disorder affecting ~2-3% of the population. This disorder involves genetic and, possibly, epigenetic risk factors. The dynamic nature of epigenetics also presents a promising avenue for identifying biomarkers associated with symptom severity, clinical progression, and treatment response in OCD. We, therefore, conducted a comprehensive case-control investigation using Illumina MethylationEPIC BeadChip, encompassing 185 OCD patients and 199 controls recruited from two distinct sites in Germany. Rigorous clinical assessments were performed by trained raters employing the Structured Clinical Interview for DSM-IV (SCID-I). We performed a robust two-step epigenome-wide association study that led to the identification of 305 differentially methylated CpG positions. Next, we validated these findings by pinpointing the optimal set of CpGs that could effectively classify individuals into their respective groups. This approach identified a subset comprising 12 CpGs that overlapped with the 305 CpGs identified in our EWAS. These 12 CpGs are close to or in genes associated with the sweet-compulsive brain hypothesis which proposes that aberrant dopaminergic transmission in the striatum may impair insulin signaling sensitivity among OCD patients. We replicated three of the 12 CpGs signals from a recent independent study conducted on the Han Chinese population, underscoring also the cross-cultural relevance of our findings. In conclusion, our study further supports the involvement of epigenetic mechanisms in the pathogenesis of OCD. By elucidating the underlying molecular alterations associated with OCD, our study contributes to advancing our understanding of this complex disorder and may ultimately improve clinical outcomes for affected individuals.

The role of the dorsal anterior cingulate cortex in obsessive-compulsive disorder

Despite extensive research efforts, the pathophysiology of obsessive-compulsive disorder (OCD) is still largely unknown. The dorsal anterior cingulate cortex (dACC) plays an important role in cognitive control and is therefore hypothesized to contribute to the pathogenesis of OCD. In this review, we aim to gain a wider understanding of the specific functions of the dACC and its role in the pathophysiology of OCD. The dACC is part of the cortico-basal ganglia-thalamo-cortical loop, where it forms connections between sensory input streams, cognitive and affective processing regions, and structures that regulate behaviour. This position facilitates a broad function for the dACC in multiple domains, which center on goal-directed behaviour and reward-based learning. When presented with a certain threatening stimulus, the dACC instructs downstream structures to select actions to respond to this particular stimulus, based on previous experiences We hypothesize that hyperactivity of the dACC may impair goal-directed behaviour in OCD patients which in turn may lead to obsessive-compulsive symptoms by creating an over-reliance on threatening stimuli and inadequate selection of neutralizing actions. The working mechanisms of cognitive behavioural therapy, serotonergic medication, repetitive transcranial magnetic stimulation and deep brain stimulation in OCD may be in part explained by the normalization of the activity of the dACC within the cortico-basal ganglia-thalamo-cortical (CBGTC) loop.

Clinical Practice Guidelines for the Use of Transcranial Direct Current Stimulation in Psychiatry.

Clinical Practice Guidelines for the Use of Transcranial Direct Current Stimulation in Psychiatry.

Cytokine profile of pediatric patients with obsessive-compulsive and/or movement disorder symptoms: A review.

Cytokines are an important modulator of the immune system and have been found to be altered significantly in many neurological and psychiatric disorders, like obsessive compulsive disorder (OCD) and movement disorders. Also, in pediatric autoimmune neuropsychiatric disorders associated with group A streptococcal infections (PANDAS), which are characterized by abrupt debut of symptoms of OCD and /or movement disorder symptoms, alterations in the immune system have been suggested. The aim of this paper was to review the current literature on the cytokine profile of pediatric patients with symptoms of OCD and/or movement disorder symptoms. A search of PubMed and Medline was performed with specific keywords to review studies measuring cytokines in pediatric patients with symptoms of OCD and/or movement disorders. Nineteen studies were found, twelve of which included a healthy control group, while four studies had control groups of children with other disorders, primarily neurological or psychiatric. One study compared cytokines measurements to reference intervals, and two studies had a longitudinal design. Many cytokines were found to have significant changes in patients with symptoms of OCD and/or movement disorders compared to both healthy controls and other control groups. Furthermore, differences were found when comparing cytokines in periods of exacerbation with periods of remission of symptoms in study participants. The cytokines that most studies with healthy control groups found to be significantly altered were TNF-α, IL-1β and IL-17. Although the exact role of these cytokines in OCD and movement disorder symptoms remains unclear, the available literature suggests a proinflammatory cytokine profile. This offers interesting perspectives on the pathogenesis of OCD and/or movement disorder symptoms in children, and further research into the implications of cytokines in neuropsychiatric disorders is warranted.

BDNF Alleviates Microglial Inhibition and Stereotypic Behaviors in a Mouse Model of Obsessive-Compulsive Disorder.

Obsessive-compulsive disorder (OCD) is a severe mental illness characterized by obsessions and compulsions. However, its underlying mechanisms remain to be elucidated. Recent studies have suggested that neuroimmune dysregulation is involved in the pathogenesis of OCD. To investigate the role of microglia in this disorder, we established a pharmacological mouse model by using the serotonin (5-HT) 1A/1B receptor agonist RU24969 to mimic monoamine dysregulation in OCD, and we examined the morphological and functional alterations of microglia in this model. We found that RU24969 treatment led to compulsive circling behavior in mice. Strikingly, we found that the density and mobility of microglia in the prelimbic cortex were much lower in RU24969-treated mice than in control mice. Moreover, the expression of cytokines and chemokines, including BDNF, IL-1β, IL-6, TNFα, CD80, CD86, MHC-I, and MHC-II, also decreased in RU24969-treated mice. Importantly, we found that injection of BDNF or induction of BDNF expression by trehalose completely reversed microglial dysfunction and reduced stereotypic behavior. These results indicate that microglial dysfunction is closely related to stereotypic behaviors in our mouse model of OCD and that BDNF could be an effective treatment for stereotypic behaviors.

Serum Claudin-5, but not Zonulin, May Be Associated with Obsessive-Compulsive Disorder.

The aim of this research was to assess serum zonulin and claudin-5 concentrations to show whether or not their eventual changes in patients with obsessive-compulsive disorder (OCD) could have etiopathogenetic importance. There was no research in the literature assessing serum zonulin and claudin-5 levels in OCD to the best of our understanding. In this study, we assumed that there may be a deterioration in serum zonulin and claudin-5 levels in OCD patients and this may affect the severity of the disease. Thirty-six OCD patients and 35 healthy controls were included in this study. The patients were administered Hamilton Depression Rating Scale (HDRS) and Yale-Brown Obsession Compulsion Scale (Y-BOCS) to determine the severity of depression and OCD, respectively. Venous blood samples were collected, and serum zonulin and claudin-5 levels were measured. The mean serum claudin-5 level was significantly higher without a significant difference between age, sex, and body mass index, whereas serum zonulin level was not different from the control group in OCD patients. In conclusion, the current research indicates that claudin-5 is enhanced in OCD patients and this finding may contribute to the role of blood-brain barrier in the pathogenesis of OCD.

STAT3 and NTRK2 Genes Predicted by the Bioinformatics Approach May Play Important Roles in the Pathogenesis of Multiple Sclerosis and Obsessive-Compulsive Disorder.

Background: There are no data available on the levels of genetic networks between obsessive–compulsive disorder (OCD) and multiple sclerosis (MS). To this point, we aimed to investigate common mechanisms and pathways using bioinformatics approaches to find novel genes that may be involved in the pathogenesis of OCD in MS. Methods: To obtain gene–gene interactions for MS and OCD, the STRING database was used. Cytoscape was then used to reconstruct and visualize graphs. Then, ToppGene and Enrichr were used to identify the main pathological processes and pathways involved in MS-OCD novel genes. Additionally, to predict transcription factors and microRNAs (miRNAs), the Enrichr database and miRDB database were used, respectively. Results: Our bioinformatics analysis showed that the signal transducer and the activator of transcription 3 (STAT3) and neurotrophic receptor tyrosine kinase 2 (NTRK2) genes had connections with 32 shared genes between MS and OCD. Furthermore, STAT3 and NTRK2 had the greatest enrichment parameters (i.e., molecular function, cellular components, and signaling pathways) among ten hub genes. Conclusions: To summarize, data from our bioinformatics analysis showed that there was a significant overlap in the genetic components of MS and OCD. The findings from this study make two contributions to future studies. First, predicted mechanisms related to STAT3 and NTRK2 in the context of MS and OCD can be investigated for pharmacological interventions. Second, predicted miRNAs related to STAT3 and NTRK2 can be tested as biomarkers in MS with OCD comorbidity. However, our study involved bioinformatics research; therefore, considerable experimental work (e.g., postmortem studies, case–control studies, and cohort studies) will need to be conducted to determine the etiology of OCD in MS from a mechanistic view.

Epigenome-wide DNA methylation in obsessive-compulsive disorder

In adult patients with obsessive-compulsive disorder (OCD), altered DNA methylation has been discerned in several candidate genes, while DNA methylation on an epigenome-wide level has been investigated in only one Chinese study so far. Here, an epigenome-wide association study (EWAS) was performed in a sample of 76 OCD patients of European ancestry (37 women, age ± SD: 33.51 ± 10.92 years) and 76 sex- and age-matched healthy controls for the first time using the Illumina MethylationEPIC BeadChip. After quality control, nine epigenome-wide significant quantitative trait methylation sites (QTMs) and 21 suggestive hits were discerned in the final sample of 68 patients and 68 controls. The top hit (cg24159721) and four other significant QTMs (cg11894324, cg01070250, cg11330075, cg15174812) map to the region of the microRNA 12136 gene (MIR12136). Two additional significant CpG sites (cg05740793, cg20450977) are located in the flanking region of the MT-RNR2 (humanin) like 8 gene (MT-RNRL8), while two further QTMs (cg16267121, cg15890734) map to the regions of the MT-RNR2 (humanin) like 3 (MT-RNRL3) and MT-RNR2 (humanin) like 2 (MT-RNRL2) genes. Provided replication of the present findings in larger samples, the identified QTMs might provide more biological insight into the pathogenesis of OCD and thereby could in the future serve as peripheral epigenetic markers of OCD risk with the potential to inform targeted preventive and therapeutic efforts.

Accelerated Brain Aging in Patients With Obsessive-Compulsive Disorder.

Obsessive-compulsive disorder (OCD) may be accompanied by an accelerated structural decline of the brain with age compared to healthy controls (HCs); however, this has yet to be proven. To answer this question, we built a brain age prediction model using mean gray matter volumes of each brain region as features, which were obtained by voxel-based morphometry derived from T1-weighted MRI scans. The prediction model was built using two Chinese Han datasets (dataset 1, N = 106 for HCs and N = 90 for patients with OCD; dataset 2, N = 270 for HCs) to evaluate its performance. Then, a new prediction model was trained using data for HCs in dataset 1 and applied to patients with OCD to investigate the brain aging trajectory. The brain-predicted age difference (brain-PAD) scores, defined as the difference between predicted brain age and chronological age, were calculated for all participants and compared between patients with matched HCs in dataset 1. It was demonstrated that the prediction model performs consistently across different datasets. Patients with OCD presented higher brain-PAD scores than matched HCs, suggesting that patients with OCD presented accelerated brain aging. In addition, brain-PAD scores were negatively correlated with the duration of illness, suggesting that brain-PAD scores might capture progressive structural brain changes. These results identified accelerated brain aging in patients with OCD for the first time and deepened our understanding of the pathogenesis of OCD.

P458. Differences in Dendritic Spine Density in Post-Mortem Brains of Individuals With Obsessive Compulsive Disorder and Healthy Controls

The cellular and molecular pathogenesis of obsessive compulsive disorder (OCD) is largely unknown, but brain imaging studies have suggested that hyperactivity in decision-making regions of the brain, specifically the orbitofrontal cortex (OFC), is associated with OCD symptoms. Recent work has shown significant differences in the expression of excitatory genes in human patients with OCD compared to unaffected comparison subjects using post-mortem samples from the University of Pittsburgh Brain Tissue Donation Program.

Associations Between Blood Levels of NLRP3 Inflammasome Components and Obsessive Compulsive Disorder.

Even though the effect of inflammation on pathogenesis of obsessive compulsive disorder (OCD) is known, information regarding the underlying mechanisms are yet to be revealed. The NLRP3 inflammasome complex is an important component of the innate immune system that initiates and mediates inflammatory response to a variety of stimuli. This study aims to inquire into a possible association between NLRP3 inflammasome complex and OCD. This case-control study included 103 participants (51 cases with OCD and 52 healthy controls). All participants were evaluated with the Yale Brown Obsessive Compulsive Scale, Hamilton Depression Scale, and Hewitt Multidimensional Perfectionism Scale. RNA and proteins were extracted from peripheral blood mononuclear cells. Expression of NLRP3 inflammasome components were determined using quantitative real-time polymerase chain reaction (PCR) and Western blotting. Levels of Serum IL-1beta and IL-18 cytokine were determined by ELISA. NEK7 and CASP1 mRNA levels were significantly higher in OCD patients, compared to controls. Pro-caspase-1 protein levels were elevated, as well. Regression analysis showed that NEK7 mRNA and pro-caspase-1 protein levels can differentiate OCD and healthy control groups. Our results provide insight into the molecular alterations that could explain the inflammation-OCD association.

Genomics of Obsessive-Compulsive Disorder-Toward Personalized Medicine in the Era of Big Data.

Pathogenesis of obsessive-compulsive disorder (OCD) mainly involves dysregulation of serotonergic neurotransmission, but a number of other factors are involved. Genetic underprints of OCD fall under the category of “common disease common variant hypothesis,” that suggests that if a disease that is heritable is common in the population (a prevalence >1–5%), then the genetic contributors—specific variations in the genetic code—will also be common in the population. Therefore, the genetic contribution in OCD is believed to come from multiple genes simultaneously and it is considered a polygenic disorder. Genomics offers a number of advanced tools to determine causal relationship between the exposure and the outcome of interest. Particularly, methods such as polygenic risk score (PRS) or Mendelian Randomization (MR) enable investigation of new pathways involved in OCD pathogenesis. This premise is also facilitated by the existence of publicly available databases that include vast study samples. Examples include population-based studies such as UK Biobank, China Kadoorie Biobank, Qatar Biobank, All of US Program sponsored by National Institute of Health or Generations launched by Yale University, as well as disease-specific databases, that include patients with OCD and co-existing pathologies, with the following examples: Psychiatric Genomics Consortium (PGC), ENIGMA OCD, The International OCD Foundation Genetics Collaborative (IOCDF-GC) or OCD Collaborative Genetic Association Study. The aim of this review is to present a comprehensive overview of the available Big Data resources for the study of OCD pathogenesis in the context of genomics and demonstrate that OCD should be considered a disorder which requires the approaches offered by personalized medicine.

Decreased Nucleus Accumbens Connectivity at Rest in Medication-Free Patients with Obsessive-Compulsive Disorder.

Background Patients with obsessive-compulsive disorder (OCD) experience deficiencies in reward processing. The investigation of the reward circuit and its essential connectivity may further clarify the pathogenesis of OCD. Methods The current research was designed to analyze the nucleus accumbens (NAc) functional connectivity at rest in medicine-free patients with OCD. Forty medication-free patients and 38 gender-, education-, and age-matched healthy controls (HCs) were recruited for resting-state functional magnetic resonance imaging. Seed-based functional connectivity (FC) was used to analyze the data. LIBSVM (library for support vector machines) was designed to identify whether altered FC could be applied to differentiate OCD. Results Patients with OCD showed remarkably decreased FC values between the left NAc and the bilateral orbitofrontal cortex (OFC) and bilateral medial prefrontal cortex (MPFC) and between the right NAc and the left OFC at rest in the reward circuit. Moreover, decreased left NAc-bilateral MPFC connectivity can be deemed as a potential biomarker to differentiate OCD from HCs with a sensitivity of 80.00% and a specificity of 76.32%. Conclusion The current results emphasize the importance of the reward circuit in the pathogenesis of OCD.

Elevated serum S100B levels in medication naïve children and adolescents with obsessive-compulsive disorder

Purpose Obsessive-compulsive disorder (OCD) is a condition characterized by obsessions and/or compulsions. S100B protein is shown to be involved in microglial activation besides intracellular signaling, intercellular communication and cell growth. The relation between S100B protein and various psychiatric disorders except OCD has been studied so far. This study aimed to analyze serum S100B levels for the first time in medication naive OCD diagnosed children and adolescents and to compare them with the control group. Materials and methods Peripheral blood S100B levels of 27 children and adolescents with OCD were compared to 27 control group subjects to assess any possible association between OCD and S100B levels. All the children and adolescents completed the child version of the Obsessive-Compulsive Inventory (OCI - CV). Results Compared to control group, higher serum S100B levels were found in OCD group (z = −2.258, p = 0.024). We also found that obsessing and washing subscales’ scores and total score of OCI - CV were statistically significantly correlated with S100B levels (respectively, r = .292, p = 0.032; r = .306, p = 0.025; r = .296, p = 0.030). Conclusions The present study’s findings are in accord with previous studies demonstrating the significance of S100B protein in other psychiatric disorders and suggesting a relation in children and adolescents with OCD for the first time. The role of S100B protein in OCD etiology and pathogenesis should be evaluated further.