Obsessive-Compulsive Disorder

1. Disease Information

Overview and Definition

Obsessive-Compulsive Disorder (OCD) is a neuropsychiatric condition characterized by unwanted obsessions (repetitive thoughts, images, or urges) and/or compulsions (repetitive behaviors or mental acts) that cause significant distress and functional impairment (jalal2023obsessive‐compulsivedisorderetiology pages 1-2, roh2023clinicaladvancesin pages 1-2). OCD affects approximately 1-3% of the general population, making it a common psychiatric disorder with substantial public health burden (jalal2023obsessive‐compulsivedisorderetiology pages 1-2, stein2025obsessivecompulsivedisorderin pages 1-2, strom2025genomewideanalysesidentify pages 1-2).

Classification and Identifiers

In the DSM-5 and ICD-11, OCD was reclassified from the anxiety disorder category to a new grouping called "Obsessive-Compulsive and Related Disorders" (OCRD), reflecting improved understanding of its distinct neurobiological substrates (jalal2023obsessive‐compulsivedisorderetiology pages 1-2, roh2023clinicaladvancesin pages 1-2, jalal2023obsessive‐compulsivedisorderetiology pages 2-3). This category includes hoarding disorder, body dysmorphic disorder, trichotillomania, and excoriation disorder (jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Diagnostic Criteria

According to DSM-5, diagnosis requires the presence of obsessions and/or compulsions that are time-consuming (taking more than one hour per day) and cause significant distress or interfere with everyday activities including social and occupational functioning (jalal2023obsessive‐compulsivedisorderetiology pages 1-2). The DSM-5 includes a specifier for insight level, recognizing that patients vary from good/fair insight to absent insight or delusional beliefs (jalal2023obsessive‐compulsivedisorderetiology pages 1-2, jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

2. Etiology

Disease Causal Factors

OCD etiology involves a complex interplay of genetic vulnerability, environmental exposures, and neurobiological mechanisms (dhiman2025hereditarypatternsand pages 1-1, roh2023clinicaladvancesin pages 1-2, liu2023earlyidentificationand pages 1-2).

Risk Factors

Genetic Risk Factors: OCD demonstrates substantial heritability. Twin-based heritability estimates range from 27-47% in adults and 45-65% in children, with pediatric-onset OCD showing higher genetic loading than adult-onset cases (dhiman2025hereditarypatternsand pages 1-1, strom2025genomewideanalysesidentify pages 1-2, liu2023earlyidentificationand pages 1-2). Family studies indicate genetic contribution of 35-50% (roh2023clinicaladvancesin pages 1-2).

The largest genome-wide association study (GWAS) meta-analysis to date, combining 53,660 OCD cases and 2,044,417 controls, identified 30 independent genome-wide significant loci (strom2025genomewideanalysesidentify pages 1-2, strom2025genomewideanalysesidentify pages 2-3). Key findings include: - Approximately 11,500 genetic variants explain 90% of OCD genetic heritability, indicating highly polygenic architecture (strom2025genomewideanalysesidentify pages 2-3) - SNP-based heritability estimated at 6.7% (SE 0.3%) assuming 1% population prevalence, with higher estimates in clinically ascertained samples (strom2025genomewideanalysesidentify pages 2-3) - Priority candidate genes include WDR6, DALRD3, and CTNND1, along with multiple genes in the major histocompatibility complex (MHC) region (strom2025genomewideanalysesidentify pages 1-2, strom2025genomewideanalysesidentify pages 3-4)

Environmental Risk Factors: While specific environmental factors remain under investigation, adverse lifetime experiences may induce neurobiological adaptations within a genetic vulnerability window (roh2023clinicaladvancesin pages 1-2). The OCDTWIN project is systematically investigating environmental risk factors through discordant monozygotic twin pairs (dhiman2025hereditarypatternsand pages 1-1).

Gene-Environment Interactions: Limited direct evidence exists for specific gene-environment interactions in OCD, though the OCDTWIN study aims to isolate unique environmental risk factors in the causal pathway while controlling for genetic influences (dhiman2025hereditarypatternsand pages 1-1).

Table: This table summarizes the major genetic findings for obsessive-compulsive disorder from recent large-scale GWAS and gene-prioritization analyses. It highlights the most important loci, candidate genes, heritability estimates, and polygenic architecture features that are most useful for a disease knowledge base.

3. Phenotypes

Symptom Dimensions

OCD symptoms are classified into partially distinct subtypes (jalal2023obsessive‐compulsivedisorderetiology pages 2-3): 1. Contamination fears and compulsive cleaning 2. Obsessive thoughts about causing harm and compulsive checking 3. Obsessions with symmetry and compulsive ordering 4. Obsessions with collecting and compulsive hoarding (now a separate disorder in DSM-5) 5. Purely obsessional subtype with unwanted thoughts about sex, violence, and blasphemy

Suggested HPO Terms: - HP:0000722 (Obsessive-compulsive behavior) - HP:0000733 (Repetitive compulsive behavior) - HP:0000723 (Restricted interests)

Phenotype Characteristics

Age of Onset: OCD demonstrates a bimodal onset with peaks at 12-14 years and 20-22 years (liu2023earlyidentificationand pages 1-2). More than 80% of OCD cases begin by early adulthood (stein2025obsessivecompulsivedisorderin pages 1-2). Half of adult patients exhibited symptoms starting in childhood or adolescence (farrell2023closingthegap pages 1-2, liu2023earlyidentificationand pages 1-2).

Severity: In community samples, most OCD cases are mild (47.0%) or very mild (27.5%), with smaller percentages designated as moderate (22.9%) or severe (2.7%) by Yale-Brown Obsessive-Compulsive Scale (stein2025obsessivecompulsivedisorderin pages 1-2).

Progression: OCD typically starts in childhood or adolescence and often persists throughout life, causing functional impairment across multiple domains (roh2023clinicaladvancesin pages 1-2). The 12-month prevalence (3.0%) is nearly as high as lifetime prevalence (4.1%), suggesting highly persistent course (stein2025obsessivecompulsivedisorderin pages 1-2).

Quality of Life Impact

OCD causes substantial disability and is among the leading causes of illness-related burden according to the World Health Organization (roh2023clinicaladvancesin pages 1-2, farrell2023closingthegap pages 1-2). Childhood onset is associated with greater OCD severity, more symptoms, higher comorbidity, and poorer prognosis relative to adult onset (farrell2023closingthegap pages 1-2).

4. Genetic/Molecular Information

Causal Genes and Pathogenic Variants

The 2025 GWAS meta-analysis identified 249 potential effector genes for OCD, with 25 classified as most likely causal candidates (strom2025genomewideanalysesidentify pages 1-2). Key genes include:

• WDR6 (2q33): WD repeat domain 6, prioritized by both TWAS-COLOC and SMR-HEIDI causality filters (strom2025genomewideanalysesidentify pages 3-4)
• DALRD3 (2q33): DALR anticodon binding domain-containing 3, also prioritized by convergent causal inference methods (strom2025genomewideanalysesidentify pages 3-4)
• CTNND1 (6p22): Catenin delta-1, implicated by three orthogonal approaches (mBAT-combo, TWAS, PWAS) with evidence for colocalization; protein downregulation in dorsolateral prefrontal cortex associated with OCD risk (Z = -4.49, P = 7.11×10⁻⁶) (strom2025genomewideanalysesidentify pages 3-4)
• MHC region genes (6p21.33): Multiple genes in the major histocompatibility complex region (strom2025genomewideanalysesidentify pages 1-2, strom2025genomewideanalysesidentify pages 2-3)

Variant Classification

The current evidence primarily derives from common variant GWAS rather than rare coding variants. The polygenic architecture suggests thousands of small-effect variants rather than high-penetrance mutations (strom2025genomewideanalysesidentify pages 2-3).

Cell Type and Tissue Enrichment

OCD genetic risk shows significant enrichment in: - Excitatory neurons in hippocampus and cerebral cortex - D1 and D2 type dopamine receptor-containing medium spiny neurons in the striatum (strom2025genomewideanalysesidentify pages 1-2, strom2025genomewideanalysesidentify pages 3-4)

Tissue enrichment analysis revealed significant signals in anterior cingulate cortex, frontal cortex, nucleus accumbens, hippocampus, caudate, putamen, hypothalamus, and cerebellum (strom2025genomewideanalysesidentify pages 3-4).

5. Environmental Information

Environmental Factors

The specific environmental contributors to OCD remain under active investigation. The OCDTWIN project is systematically evaluating early life exposures including perinatal variables, psychosocial stressors, and health-related information through register linkages (dhiman2025hereditarypatternsand pages 1-1).

Lifestyle Factors

Limited specific data available from retrieved sources.

6. Mechanism / Pathophysiology

Molecular Pathways

The dominant pathophysiological model implicates dysfunction in cortico-striato-thalamo-cortical (CSTC) circuits (jalal2023obsessive‐compulsivedisorderetiology pages 1-2, roh2023clinicaladvancesin pages 1-2, jalal2023obsessive‐compulsivedisorderetiology pages 2-3). These parallel circuits are responsible for reward and motivational processes, executive function, motor and response inhibition, and habit-based behavior (jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Key CSTC circuits include (jalal2023obsessive‐compulsivedisorderetiology pages 2-3): 1. Affective circuit: Projects from anterior cingulate cortex (ACC) and ventromedial prefrontal cortex (vmPFC) to nucleus accumbens, involved in emotion and reward processing 2. Dorsal cognitive circuit: Projects from dorsolateral prefrontal cortex (dlPFC) to caudate nucleus, pertinent to executive function and working memory 3. Ventral cognitive circuit: Projects from anterolateral orbitofrontal cortex to putamen, responsible for motor and response inhibition 4. Sensorimotor circuit: Projects from premotor cortical regions to putamen, involved in habit-based behavior

Neurochemical Systems

Serotonin: Dysfunction in serotonergic neurotransmission is strongly implicated, as evidenced by the efficacy of selective serotonin reuptake inhibitors (SSRIs) (roh2023clinicaladvancesin pages 1-2, jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Dopamine: Dopaminergic systems play an important role, particularly in striatal function and the generation of compulsive behaviors (jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Glutamate: Glutamatergic dysregulation within CSTC circuits is increasingly recognized as contributing to OCD pathophysiology (jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Cellular Processes

OCD involves aberrant activity within CSTC circuits, with evidence of overactivity in orbitofrontal cortex and striatum that can normalize following successful pharmacological and psychological treatment (jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Suggested GO Terms: - GO:0007165 (Signal transduction) - GO:0007268 (Chemical synaptic transmission) - GO:0042493 (Response to drug) - GO:0050890 (Cognition)

Suggested CL Terms: - CL:0000540 (Neuron) - CL:0000100 (Motor neuron) - CL:0000679 (Glutamatergic neuron)

7. Anatomical Structures Affected

Organ and System Level

Primary Organs: Central nervous system, particularly brain regions within CSTC circuits

Brain Systems: - Orbitofrontal cortex (OFC) - Anterior cingulate cortex (ACC) - Dorsolateral prefrontal cortex (dlPFC) - Ventromedial prefrontal cortex (vmPFC) - Striatum (caudate nucleus, putamen, nucleus accumbens) - Thalamus - Cerebellum (jalal2023obsessive‐compulsivedisorderetiology pages 2-3, strom2025genomewideanalysesidentify pages 3-4)

Cell and Tissue Level

Cell Types Affected: - Excitatory neurons in hippocampus and cortex - D1 and D2 dopamine receptor-containing medium spiny neurons in striatum (strom2025genomewideanalysesidentify pages 1-2, strom2025genomewideanalysesidentify pages 3-4)

Suggested UBERON Terms: - UBERON:0000955 (Brain) - UBERON:0002037 (Cerebellum) - UBERON:0001950 (Neocortex) - UBERON:0002435 (Striatum) - UBERON:0001897 (Thalamus)

8. Temporal Development

Onset

Typical Age of Onset: Bimodal distribution with peaks at 12-14 years and 20-22 years (liu2023earlyidentificationand pages 1-2). More than 80% of cases begin by early adulthood, with more than half of adult OCD patients having onset in childhood or adolescence (stein2025obsessivecompulsivedisorderin pages 1-2, farrell2023closingthegap pages 1-2).

Onset Pattern: Can be acute, subacute, or insidious. Childhood-onset OCD is associated with greater severity and higher genetic loading compared to adult-onset (farrell2023closingthegap pages 1-2, liu2023earlyidentificationand pages 1-2).

Progression

Disease Course: OCD typically demonstrates a chronic course with high persistence. The 12-month prevalence (3.0%) nearly equals lifetime prevalence (4.1%), suggesting minimal spontaneous remission (stein2025obsessivecompulsivedisorderin pages 1-2). Studies in youth suggest a higher percentage have an episodic course compared to adults (liu2023earlyidentificationand pages 1-2).

Duration: Delayed diagnosis is common, with a gap between onset and diagnosis of approximately 7-10 years in adults and more than 2 years in children (liu2023earlyidentificationand pages 1-2). Australian data suggest more than 9 years of untreated illness for OCD (farrell2023closingthegap pages 1-2).

9. Inheritance and Population

Epidemiology

Prevalence: Lifetime prevalence across 10 countries in World Mental Health surveys is 4.1%, with 12-month prevalence of 3.0% (stein2025obsessivecompulsivedisorderin pages 1-2). Estimates from literature range from 1-3% of the general population (jalal2023obsessive‐compulsivedisorderetiology pages 1-2, strom2025genomewideanalysesidentify pages 1-2).

Incidence: Pediatric-onset OCD affects approximately 2-4% of children and adolescents (liu2023earlyidentificationand pages 1-2).

Inheritance Pattern

OCD demonstrates polygenic inheritance with moderate heritability. Twin-based heritability: 27-47% in adults, 45-65% in children (dhiman2025hereditarypatternsand pages 1-1, strom2025genomewideanalysesidentify pages 1-2). Family studies show OCD is more prevalent in first-degree relatives of affected individuals (farrell2023closingthegap pages 1-2).

Population Demographics

Age Distribution: Bimodal onset with peaks in adolescence (12-14 years) and young adulthood (20-22 years) (liu2023earlyidentificationand pages 1-2).

Sex Ratio: Available sources did not provide definitive male:female ratios.

Geographic Distribution: OCD appears cross-culturally prevalent with relatively consistent rates across high-income countries (HICs) and low-middle income countries (LMICs), though treatment rates are much higher in HICs (40.5%) than LMICs (7.0%) (stein2025obsessivecompulsivedisorderin pages 1-2).

10. Diagnostics

Clinical Criteria

DSM-5 Diagnostic Criteria: Presence of obsessions and/or compulsions that are time-consuming (>1 hour/day) and cause significant distress or functional impairment. Symptoms must not be attributable to other mental or physical disorders (jalal2023obsessive‐compulsivedisorderetiology pages 1-2).

Differential Diagnosis: Must distinguish from other obsessive-compulsive and related disorders, anxiety disorders, and psychotic disorders. Level of insight distinguishes OCD with poor/absent insight from primary psychotic illness (jalal2023obsessive‐compulsivedisorderetiology pages 1-2).

Clinical Tests

Severity Assessment: Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) is the standard severity measure (stein2025obsessivecompulsivedisorderin pages 1-2).

Imaging Studies: Neuroimaging reveals functional abnormalities in CSTC circuits, particularly in orbitofrontal cortex, anterior cingulate cortex, striatum, and thalamus (jalal2023obsessive‐compulsivedisorderetiology pages 2-3). Both structural MRI and functional MRI demonstrate aberrant CSTC connectivity and activity (jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Genetic Testing

While specific genes have been identified through GWAS, genetic testing is not currently part of routine clinical diagnosis given the highly polygenic architecture. Research applications include whole exome sequencing and genome-wide genotyping for risk prediction and mechanistic studies (strom2025genomewideanalysesidentify pages 1-2).

11. Outcome/Prognosis

Disease Course and Morbidity

OCD is highly persistent, with 12-month prevalence nearly matching lifetime prevalence (stein2025obsessivecompulsivedisorderin pages 1-2). The condition causes substantial functional impairment across academic, occupational, and social domains (farrell2023closingthegap pages 1-2). Childhood onset is associated with greater severity, more symptoms, and poorer prognosis than adult onset (farrell2023closingthegap pages 1-2).

Quality of Life

OCD is ranked among the leading causes of illness-related disability by the World Health Organization (roh2023clinicaladvancesin pages 1-2). The disorder significantly impacts daily functioning, with severe cases experiencing substantial disability in occupational and social domains (farrell2023closingthegap pages 1-2).

Treatment Response

Only 19.8% of respondents with OCD in World Mental Health surveys received any mental health treatment in the past year (stein2025obsessivecompulsivedisorderin pages 1-2). Approximately 50% of OCD patients do not respond adequately to initial treatments (huang2025advancingobsessive–compulsivedisorder pages 1-2). Treatment adherence during exposure and response prevention predicts both short-term and long-term outcomes (farrell2023closingthegap pages 1-2).

12. Treatment

Pharmacotherapy

First-Line: Selective serotonin reuptake inhibitors (SSRIs) including fluoxetine, sertraline, fluvoxamine, paroxetine, and escitalopram are considered first-line pharmacotherapy (roh2023clinicaladvancesin pages 1-2, huang2025advancingobsessive–compulsivedisorder pages 1-2). SSRIs modulate serotonergic neurotransmission and downstream CSTC circuit activity (roh2023clinicaladvancesin pages 1-2).

Augmentation: Atypical antipsychotics are used for augmentation in SSRI partial responders, particularly those with tic-related presentations (roh2023clinicaladvancesin pages 1-2).

Psychotherapy

Cognitive Behavioral Therapy with Exposure and Response Prevention (CBT-ERP): Gold-standard psychological treatment involving systematic exposure to obsessional triggers with prevention of compulsive responses (roh2023clinicaladvancesin pages 1-2, farrell2023closingthegap pages 1-2). CBT-ERP promotes inhibitory learning, fear extinction, and improved cognitive control (farrell2023closingthegap pages 1-2).

Treatment Modalities: Delivered through individual therapy, family-based approaches, group therapy, and internet-delivered formats. Intensive or concentrated ERP (over consecutive days) may be beneficial for severe or treatment-resistant cases (farrell2023closingthegap pages 1-2).

Advanced Therapeutics

Neuromodulation: Transcranial magnetic stimulation (TMS) and deep brain stimulation (DBS) targeting CSTC circuit nodes are used for treatment-refractory OCD (roh2023clinicaladvancesin pages 1-2, huang2025advancingobsessive–compulsivedisorder pages 1-2).

Neurosurgical Interventions: Ablative procedures such as anterior cingulotomy are reserved for severe, treatment-refractory cases (jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Treatment Strategy

Staged-care models match treatment intensity to illness severity, comorbidity burden, and prior treatment response. This approach aims to deliver "right care, first time" and close treatment gaps (farrell2023closingthegap pages 1-2).

Suggested MAXO Terms: - MAXO:0000011 (Psychotherapy) - MAXO:0000058 (Pharmacotherapy) - MAXO:0001298 (Cognitive behavioral therapy)

Table: This table summarizes current OCD treatment strategies across first-line, second-line, experimental, and treatment-resistant settings. It highlights mechanisms, approximate evidence strength, and clinically relevant outcome patterns from recent reviews and studies.

13. Prevention

Secondary Prevention

Early identification and intervention in pediatric OCD is critical, as delayed treatment is associated with worse prognosis (liu2023earlyidentificationand pages 1-2). Interventions focus on preventing conversion of obsessive-compulsive symptoms into full-blown OCD (liu2023earlyidentificationand pages 1-2).

Tertiary Prevention

Focuses on alleviating mild to moderate OCD and preventing complications, though interventions for comorbidities remain in their infancy (liu2023earlyidentificationand pages 1-2).

Screening

Systematic screening programs for OCD are not currently widespread. The duration of untreated OCD remains among the highest of all psychiatric disorders, highlighting need for improved early detection (liu2023earlyidentificationand pages 1-2).

14. Other Species / Natural Disease

Limited information available in retrieved sources regarding naturally occurring OCD in other species.

15. Model Organisms

Genetic Models

Multiple transgenic mouse models have been developed to study OCD mechanisms (huang2025advancingobsessive–compulsivedisorder pages 1-2):

Key Mouse Models: - Hoxb8-KO: Excessive grooming/self-injury phenotype - Slc1a1-KO: Glutamatergic dysfunction model - Sapap3-KO: Well-established compulsive grooming model with corticostriatal synaptic abnormalities - Slitrk5-KO: Excessive grooming and anxiety-like behaviors - Spred2-KO: Repetitive grooming/compulsive-like behavior

Circuit Models

Optogenetic stimulation of orbitofrontal cortex-ventromedial striatum (OFC-VMS) connections can induce OCD-like grooming behaviors in mice, supporting the CSTC circuit model (jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Zebrafish Models

Zebrafish models with altered slitrk5a demonstrate OCD-like "checking" behaviors, useful for high-throughput screening (huang2025advancingobsessive–compulsivedisorder pages 1-2).

Model Limitations

No single model captures the full human OCD syndrome, particularly intrusive obsessions, symptom dimensions, fluctuating insight, and comorbidity patterns (huang2025advancingobsessive–compulsivedisorder pages 1-2, jalal2023obsessive‐compulsivedisorderetiology pages 2-3).

Table: This table summarizes major animal models used in obsessive-compulsive disorder research, emphasizing transgenic mouse lines and zebrafish models mentioned in the available sources. It is useful for comparing each model’s phenotypes, implicated circuits, translational uses, and major limitations.

Summary

Obsessive-Compulsive Disorder is a common, chronic neuropsychiatric disorder affecting 1-3% of the population with onset typically in childhood, adolescence, or young adulthood. The condition demonstrates substantial heritability (27-47% in adults, 45-65% in children) with highly polygenic architecture involving thousands of genetic variants. The largest GWAS identified 30 genome-wide significant loci and prioritized key genes including WDR6, DALRD3, and CTNND1.

OCD pathophysiology centers on dysfunction in cortico-striato-thalamo-cortical (CSTC) circuits involving orbitofrontal cortex, anterior cingulate cortex, striatum, and thalamus, with dysregulation of serotonergic, dopaminergic, and glutamatergic neurotransmission. Genetic risk is enriched in excitatory neurons of hippocampus and cortex, and dopamine receptor-containing medium spiny neurons in striatum.

First-line treatments include cognitive behavioral therapy with exposure and response prevention (CBT-ERP) and selective serotonin reuptake inhibitors (SSRIs), though approximately 50% of patients show inadequate response to initial interventions. Novel treatments include neuromodulation (TMS, DBS) for refractory cases. Staged-care models aim to match treatment intensity to clinical severity and prior response.

OCD causes substantial functional impairment and disability, with only 19.8% of affected individuals receiving treatment in the past year globally. Early identification and intervention are critical, particularly in pediatric-onset cases which demonstrate higher genetic loading and potentially worse prognosis without adequate treatment.

References

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4. (strom2025genomewideanalysesidentify pages 1-2): Nora I. Strom, Zachary F. Gerring, Marco Galimberti, Dongmei Yu, Matthew W. Halvorsen, Abdel Abdellaoui, Cristina Rodriguez-Fontenla, Julia M. Sealock, Tim Bigdeli, Jonathan R. Coleman, Behrang Mahjani, Jackson G. Thorp, Katharina Bey, Christie L. Burton, Jurjen J. Luykx, Gwyneth Zai, Silvia Alemany, Christine Andre, Kathleen D. Askland, Julia Bäckman, Nerisa Banaj, Cristina Barlassina, Judith Becker Nissen, O. Joseph Bienvenu, Donald Black, Michael H. Bloch, Sigrid Børte, Rosa Bosch, Michael Breen, Brian P. Brennan, Helena Brentani, Joseph D. Buxbaum, Jonas Bybjerg-Grauholm, Enda M. Byrne, Judit Cabana-Dominguez, Beatriz Camarena, Adrian Camarena, Carolina Cappi, Angel Carracedo, Miguel Casas, Maria Cristina Cavallini, Valentina Ciullo, Edwin H. Cook, Jesse Crosby, Bernadette A. Cullen, Elles J. De Schipper, Richard Delorme, Srdjan Djurovic, Jason A. Elias, Xavier Estivill, Martha J. Falkenstein, Bengt T. Fundin, Lauryn Garner, Christina Gironda, Fernando S. Goes, Marco A. Grados, Jakob Grove, Wei Guo, Jan Haavik, Kristen Hagen, Kelly Harrington, Alexandra Havdahl, Kira D. Höffler, Ana G. Hounie, Donald Hucks, Christina Hultman, Magdalena Janecka, Eric Jenike, Elinor K. Karlsson, Kara Kelley, Julia Klawohn, Janice E. Krasnow, Kristi Krebs, Christoph Lange, Nuria Lanzagorta, Daniel Levey, Kerstin Lindblad-Toh, Fabio Macciardi, Brion Maher, Brittany Mathes, Evonne McArthur, Nathaniel McGregor, Nicole C. McLaughlin, Sandra Meier, Euripedes C. Miguel, Maureen Mulhern, Paul S. Nestadt, Erika L. Nurmi, Kevin S. O’Connell, Lisa Osiecki, Olga Therese Ousdal, Teemu Palviainen, Nancy L. Pedersen, Fabrizio Piras, Federica Piras, Sriramya Potluri, Raquel Rabionet, Alfredo Ramirez, Scott Rauch, Abraham Reichenberg, Mark A. Riddle, Stephan Ripke, Maria C. Rosário, Aline S. Sampaio, Miriam A. Schiele, Anne Heidi Skogholt, Laura G. Sloofman, Jan Smit, María Soler Artigas, Laurent F. Thomas, Eric Tifft, Homero Vallada, Nathanial van Kirk, Jeremy Veenstra-VanderWeele, Nienke N. Vulink, Christopher P. Walker, Ying Wang, Jens R. Wendland, Bendik S. Winsvold, Yin Yao, Hang Zhou, Andres Metspalu, Tõnu Esko, Reedik Mägi, Mari Nelis, Georgi Hudjashov, Chris German, Arpana Agrawal, Pino Alonso, Götz Berberich, Kathleen K. Bucholz, Cynthia M. Bulik, Danielle Cath, Damiaan Denys, Valsamma Eapen, Howard Edenberg, Peter Falkai, Thomas V. Fernandez, Abby J. Fyer, J. M. Gaziano, Dan A. Geller, Hans J. Grabe, Benjamin D. Greenberg, Gregory L. Hanna, Ian B. Hickie, David M. Hougaard, Norbert Kathmann, James Kennedy, Dongbing Lai, Mikael Landén, Stéphanie Le Hellard, Marion Leboyer, Christine Lochner, James T. McCracken, Sarah E. Medland, Preben B. Mortensen, Benjamin M. Neale, Humberto Nicolini, Merete Nordentoft, Michele Pato, Carlos Pato, David L. Pauls, John Piacentini, Christopher Pittenger, Danielle Posthuma, Josep Antoni Ramos-Quiroga, Steven A. Rasmussen, Margaret A. Richter, David R. Rosenberg, Stephan Ruhrmann, Jack F. Samuels, Sven Sandin, Paul Sandor, Gianfranco Spalletta, Dan J. Stein, S. Evelyn Stewart, Eric A. Storch, Barbara E. Stranger, Maurizio Turiel, Thomas Werge, Ole A. Andreassen, Anders D. Børglum, Susanne Walitza, Kristian Hveem, Bjarne K. Hansen, Christian Rück, Nicholas G. Martin, Lili Milani, Ole Mors, Ted Reichborn-Kjennerud, Marta Ribasés, Gerd Kvale, David Mataix-Cols, Katharina Domschke, Edna Grünblatt, Michael Wagner, John-Anker Zwart, Gerome Breen, Gerald Nestadt, Jaakko Kaprio, Paul D. Arnold, Dorothy E. Grice, James A. Knowles, Helga Ask, Karin J. Verweij, Lea K. Davis, Dirk J. Smit, James J. Crowley, Jeremiah M. Scharf, Murray B. Stein, Joel Gelernter, Carol A. Mathews, Eske M. Derks, and Manuel Mattheisen. Genome-wide analyses identify 30 loci associated with obsessive–compulsive disorder. Nature Genetics, 57:1389-1401, May 2025. URL: https://doi.org/10.1038/s41588-025-02189-z, doi:10.1038/s41588-025-02189-z. This article has 70 citations and is from a highest quality peer-reviewed journal.

5. (jalal2023obsessive‐compulsivedisorderetiology pages 2-3): Baland Jalal, Samuel R. Chamberlain, and Barbara J. Sahakian. Obsessive‐compulsive disorder: etiology, neuropathology, and cognitive dysfunction. Brain and Behavior, May 2023. URL: https://doi.org/10.1002/brb3.3000, doi:10.1002/brb3.3000. This article has 162 citations and is from a peer-reviewed journal.

6. (dhiman2025hereditarypatternsand pages 1-1): Abhinay Dhiman, Sidharth Mehan, Zuber Khan, Aarti Tiwari, Ghanshyam Das Gupta, and Acharan Singh Narula. Hereditary patterns and genetic associations in obsessive-compulsive disorder (ocd): neuropsychiatric insights, genetic influences, and treatment perspectives. Mar 2025. URL: https://doi.org/10.2174/0115665232316708240828063527, doi:10.2174/0115665232316708240828063527. This article has 8 citations and is from a peer-reviewed journal.

7. (liu2023earlyidentificationand pages 1-2): Xingyu Liu and Qing Fan. Early identification and intervention in pediatric obsessive-compulsive disorder. Brain Sciences, 13:399, Feb 2023. URL: https://doi.org/10.3390/brainsci13030399, doi:10.3390/brainsci13030399. This article has 25 citations.

8. (strom2025genomewideanalysesidentify pages 2-3): Nora I. Strom, Zachary F. Gerring, Marco Galimberti, Dongmei Yu, Matthew W. Halvorsen, Abdel Abdellaoui, Cristina Rodriguez-Fontenla, Julia M. Sealock, Tim Bigdeli, Jonathan R. Coleman, Behrang Mahjani, Jackson G. Thorp, Katharina Bey, Christie L. Burton, Jurjen J. Luykx, Gwyneth Zai, Silvia Alemany, Christine Andre, Kathleen D. Askland, Julia Bäckman, Nerisa Banaj, Cristina Barlassina, Judith Becker Nissen, O. Joseph Bienvenu, Donald Black, Michael H. Bloch, Sigrid Børte, Rosa Bosch, Michael Breen, Brian P. Brennan, Helena Brentani, Joseph D. Buxbaum, Jonas Bybjerg-Grauholm, Enda M. Byrne, Judit Cabana-Dominguez, Beatriz Camarena, Adrian Camarena, Carolina Cappi, Angel Carracedo, Miguel Casas, Maria Cristina Cavallini, Valentina Ciullo, Edwin H. Cook, Jesse Crosby, Bernadette A. Cullen, Elles J. De Schipper, Richard Delorme, Srdjan Djurovic, Jason A. Elias, Xavier Estivill, Martha J. Falkenstein, Bengt T. Fundin, Lauryn Garner, Christina Gironda, Fernando S. Goes, Marco A. Grados, Jakob Grove, Wei Guo, Jan Haavik, Kristen Hagen, Kelly Harrington, Alexandra Havdahl, Kira D. Höffler, Ana G. Hounie, Donald Hucks, Christina Hultman, Magdalena Janecka, Eric Jenike, Elinor K. Karlsson, Kara Kelley, Julia Klawohn, Janice E. Krasnow, Kristi Krebs, Christoph Lange, Nuria Lanzagorta, Daniel Levey, Kerstin Lindblad-Toh, Fabio Macciardi, Brion Maher, Brittany Mathes, Evonne McArthur, Nathaniel McGregor, Nicole C. McLaughlin, Sandra Meier, Euripedes C. Miguel, Maureen Mulhern, Paul S. Nestadt, Erika L. Nurmi, Kevin S. O’Connell, Lisa Osiecki, Olga Therese Ousdal, Teemu Palviainen, Nancy L. Pedersen, Fabrizio Piras, Federica Piras, Sriramya Potluri, Raquel Rabionet, Alfredo Ramirez, Scott Rauch, Abraham Reichenberg, Mark A. Riddle, Stephan Ripke, Maria C. Rosário, Aline S. Sampaio, Miriam A. Schiele, Anne Heidi Skogholt, Laura G. Sloofman, Jan Smit, María Soler Artigas, Laurent F. Thomas, Eric Tifft, Homero Vallada, Nathanial van Kirk, Jeremy Veenstra-VanderWeele, Nienke N. Vulink, Christopher P. Walker, Ying Wang, Jens R. Wendland, Bendik S. Winsvold, Yin Yao, Hang Zhou, Andres Metspalu, Tõnu Esko, Reedik Mägi, Mari Nelis, Georgi Hudjashov, Chris German, Arpana Agrawal, Pino Alonso, Götz Berberich, Kathleen K. Bucholz, Cynthia M. Bulik, Danielle Cath, Damiaan Denys, Valsamma Eapen, Howard Edenberg, Peter Falkai, Thomas V. Fernandez, Abby J. Fyer, J. M. Gaziano, Dan A. Geller, Hans J. Grabe, Benjamin D. Greenberg, Gregory L. Hanna, Ian B. Hickie, David M. Hougaard, Norbert Kathmann, James Kennedy, Dongbing Lai, Mikael Landén, Stéphanie Le Hellard, Marion Leboyer, Christine Lochner, James T. McCracken, Sarah E. Medland, Preben B. Mortensen, Benjamin M. Neale, Humberto Nicolini, Merete Nordentoft, Michele Pato, Carlos Pato, David L. Pauls, John Piacentini, Christopher Pittenger, Danielle Posthuma, Josep Antoni Ramos-Quiroga, Steven A. Rasmussen, Margaret A. Richter, David R. Rosenberg, Stephan Ruhrmann, Jack F. Samuels, Sven Sandin, Paul Sandor, Gianfranco Spalletta, Dan J. Stein, S. Evelyn Stewart, Eric A. Storch, Barbara E. Stranger, Maurizio Turiel, Thomas Werge, Ole A. Andreassen, Anders D. Børglum, Susanne Walitza, Kristian Hveem, Bjarne K. Hansen, Christian Rück, Nicholas G. Martin, Lili Milani, Ole Mors, Ted Reichborn-Kjennerud, Marta Ribasés, Gerd Kvale, David Mataix-Cols, Katharina Domschke, Edna Grünblatt, Michael Wagner, John-Anker Zwart, Gerome Breen, Gerald Nestadt, Jaakko Kaprio, Paul D. Arnold, Dorothy E. Grice, James A. Knowles, Helga Ask, Karin J. Verweij, Lea K. Davis, Dirk J. Smit, James J. Crowley, Jeremiah M. Scharf, Murray B. Stein, Joel Gelernter, Carol A. Mathews, Eske M. Derks, and Manuel Mattheisen. Genome-wide analyses identify 30 loci associated with obsessive–compulsive disorder. Nature Genetics, 57:1389-1401, May 2025. URL: https://doi.org/10.1038/s41588-025-02189-z, doi:10.1038/s41588-025-02189-z. This article has 70 citations and is from a highest quality peer-reviewed journal.

9. (strom2025genomewideanalysesidentify pages 3-4): Nora I. Strom, Zachary F. Gerring, Marco Galimberti, Dongmei Yu, Matthew W. Halvorsen, Abdel Abdellaoui, Cristina Rodriguez-Fontenla, Julia M. Sealock, Tim Bigdeli, Jonathan R. Coleman, Behrang Mahjani, Jackson G. Thorp, Katharina Bey, Christie L. Burton, Jurjen J. Luykx, Gwyneth Zai, Silvia Alemany, Christine Andre, Kathleen D. Askland, Julia Bäckman, Nerisa Banaj, Cristina Barlassina, Judith Becker Nissen, O. Joseph Bienvenu, Donald Black, Michael H. Bloch, Sigrid Børte, Rosa Bosch, Michael Breen, Brian P. Brennan, Helena Brentani, Joseph D. Buxbaum, Jonas Bybjerg-Grauholm, Enda M. Byrne, Judit Cabana-Dominguez, Beatriz Camarena, Adrian Camarena, Carolina Cappi, Angel Carracedo, Miguel Casas, Maria Cristina Cavallini, Valentina Ciullo, Edwin H. Cook, Jesse Crosby, Bernadette A. Cullen, Elles J. De Schipper, Richard Delorme, Srdjan Djurovic, Jason A. Elias, Xavier Estivill, Martha J. Falkenstein, Bengt T. Fundin, Lauryn Garner, Christina Gironda, Fernando S. Goes, Marco A. Grados, Jakob Grove, Wei Guo, Jan Haavik, Kristen Hagen, Kelly Harrington, Alexandra Havdahl, Kira D. Höffler, Ana G. Hounie, Donald Hucks, Christina Hultman, Magdalena Janecka, Eric Jenike, Elinor K. Karlsson, Kara Kelley, Julia Klawohn, Janice E. Krasnow, Kristi Krebs, Christoph Lange, Nuria Lanzagorta, Daniel Levey, Kerstin Lindblad-Toh, Fabio Macciardi, Brion Maher, Brittany Mathes, Evonne McArthur, Nathaniel McGregor, Nicole C. McLaughlin, Sandra Meier, Euripedes C. Miguel, Maureen Mulhern, Paul S. Nestadt, Erika L. Nurmi, Kevin S. O’Connell, Lisa Osiecki, Olga Therese Ousdal, Teemu Palviainen, Nancy L. Pedersen, Fabrizio Piras, Federica Piras, Sriramya Potluri, Raquel Rabionet, Alfredo Ramirez, Scott Rauch, Abraham Reichenberg, Mark A. Riddle, Stephan Ripke, Maria C. Rosário, Aline S. Sampaio, Miriam A. Schiele, Anne Heidi Skogholt, Laura G. Sloofman, Jan Smit, María Soler Artigas, Laurent F. Thomas, Eric Tifft, Homero Vallada, Nathanial van Kirk, Jeremy Veenstra-VanderWeele, Nienke N. Vulink, Christopher P. Walker, Ying Wang, Jens R. Wendland, Bendik S. Winsvold, Yin Yao, Hang Zhou, Andres Metspalu, Tõnu Esko, Reedik Mägi, Mari Nelis, Georgi Hudjashov, Chris German, Arpana Agrawal, Pino Alonso, Götz Berberich, Kathleen K. Bucholz, Cynthia M. Bulik, Danielle Cath, Damiaan Denys, Valsamma Eapen, Howard Edenberg, Peter Falkai, Thomas V. Fernandez, Abby J. Fyer, J. M. Gaziano, Dan A. Geller, Hans J. Grabe, Benjamin D. Greenberg, Gregory L. Hanna, Ian B. Hickie, David M. Hougaard, Norbert Kathmann, James Kennedy, Dongbing Lai, Mikael Landén, Stéphanie Le Hellard, Marion Leboyer, Christine Lochner, James T. McCracken, Sarah E. Medland, Preben B. Mortensen, Benjamin M. Neale, Humberto Nicolini, Merete Nordentoft, Michele Pato, Carlos Pato, David L. Pauls, John Piacentini, Christopher Pittenger, Danielle Posthuma, Josep Antoni Ramos-Quiroga, Steven A. Rasmussen, Margaret A. Richter, David R. Rosenberg, Stephan Ruhrmann, Jack F. Samuels, Sven Sandin, Paul Sandor, Gianfranco Spalletta, Dan J. Stein, S. Evelyn Stewart, Eric A. Storch, Barbara E. Stranger, Maurizio Turiel, Thomas Werge, Ole A. Andreassen, Anders D. Børglum, Susanne Walitza, Kristian Hveem, Bjarne K. Hansen, Christian Rück, Nicholas G. Martin, Lili Milani, Ole Mors, Ted Reichborn-Kjennerud, Marta Ribasés, Gerd Kvale, David Mataix-Cols, Katharina Domschke, Edna Grünblatt, Michael Wagner, John-Anker Zwart, Gerome Breen, Gerald Nestadt, Jaakko Kaprio, Paul D. Arnold, Dorothy E. Grice, James A. Knowles, Helga Ask, Karin J. Verweij, Lea K. Davis, Dirk J. Smit, James J. Crowley, Jeremiah M. Scharf, Murray B. Stein, Joel Gelernter, Carol A. Mathews, Eske M. Derks, and Manuel Mattheisen. Genome-wide analyses identify 30 loci associated with obsessive–compulsive disorder. Nature Genetics, 57:1389-1401, May 2025. URL: https://doi.org/10.1038/s41588-025-02189-z, doi:10.1038/s41588-025-02189-z. This article has 70 citations and is from a highest quality peer-reviewed journal.

10. (farrell2023closingthegap pages 1-2): Lara J. Farrell, Allison M. Waters, Eric A. Storch, Gabrielle Simcock, Iain E. Perkes, Jessica R. Grisham, Katelyn M. Dyason, and Thomas H. Ollendick. Closing the gap for children with ocd: a staged-care model of cognitive behavioural therapy with exposure and response prevention. Clinical Child and Family Psychology Review, 26:642-664, Jul 2023. URL: https://doi.org/10.1007/s10567-023-00439-2, doi:10.1007/s10567-023-00439-2. This article has 32 citations and is from a domain leading peer-reviewed journal.

11. (huang2025advancingobsessive–compulsivedisorder pages 1-2): Xinyuejia Huang, Linglong Xiao, Mengqi Wang, Yang Wu, Hao Deng, and Wei Wang. Advancing obsessive–compulsive disorder research: insights from transgenic animal models and innovative therapies. Brain Sciences, 15:43, Jan 2025. URL: https://doi.org/10.3390/brainsci15010043, doi:10.3390/brainsci15010043. This article has 1 citations.

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