Obsessive–compulsive disorder: an integrative genetic and neurobiological perspective
Key Points Obsessive–compulsive disorder (OCD) is a phenotypically complex multidimensional neuropsychiatric disorder. Family and twin studies provide definitive evidence that genetic and environmental factors can increase risk of the disorder. Candidate gene and genome-wide association studies prov...
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description | Key Points
Obsessive–compulsive disorder (OCD) is a phenotypically complex multidimensional neuropsychiatric disorder.
Family and twin studies provide definitive evidence that genetic and environmental factors can increase risk of the disorder.
Candidate gene and genome-wide association studies provide strong suggestive evidence that genes in the serotonergic, dopaminergic and glutamatergic systems confer risk for the manifestation of OCD.
Imaging studies as well as neuropsychological and treatment studies have implicated frontal–subcortical circuits in the pathophysiology of OCD.
A cortico–striato–thalamo–cortical circuit is the prevailing model regarding the neural and pathophysiological underpinnings of OCD.
The prevailing treatments include both pharmacological agents (selective serotonin-reuptake inhibitors) and cognitive behavioural therapy (CBT), with CBT and/or a combination of pharmacological and CBT being the most efficacious.
Animal studies provide strong evidence for the involvement of the glutamatergic system in the expression of OCD-like behaviours.
A model incorporating both genetic and epigenetic mechanisms in the manifestation of OCD is suggested as a heuristic for the pathophysiology of OCD.
Obsessive–compulsive disorder has been scrutinized in many genetic, neuropsychological and neuroimaging studies. Pauls and colleagues provide an overview of our current understanding of the vulnerability factors, triggers and mechanisms underlying this devastating condition.
Obsessive–compulsive disorder (OCD) is characterized by repetitive thoughts and behaviours that are experienced as unwanted. Family and twin studies have demonstrated that OCD is a multifactorial familial condition that involves both polygenic and environmental risk factors. Neuroimaging studies have implicated the cortico–striato–thalamo–cortical circuit in the pathophysiology of the disorder, which is supported by the observation of specific neuropsychological impairments in patients with OCD, mainly in executive functions. Genetic studies indicate that genes affecting the serotonergic, dopaminergic and glutamatergic systems, and the interaction between them, play a crucial part in the functioning of this circuit. Environmental factors such as adverse perinatal events, psychological trauma and neurological trauma may modify the expression of risk genes and, hence, trigger the manifestation of obsessive–compulsive behaviours. |
doi_str_mv | 10.1038/nrn3746 |
format | Article |
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Obsessive–compulsive disorder (OCD) is a phenotypically complex multidimensional neuropsychiatric disorder.
Family and twin studies provide definitive evidence that genetic and environmental factors can increase risk of the disorder.
Candidate gene and genome-wide association studies provide strong suggestive evidence that genes in the serotonergic, dopaminergic and glutamatergic systems confer risk for the manifestation of OCD.
Imaging studies as well as neuropsychological and treatment studies have implicated frontal–subcortical circuits in the pathophysiology of OCD.
A cortico–striato–thalamo–cortical circuit is the prevailing model regarding the neural and pathophysiological underpinnings of OCD.
The prevailing treatments include both pharmacological agents (selective serotonin-reuptake inhibitors) and cognitive behavioural therapy (CBT), with CBT and/or a combination of pharmacological and CBT being the most efficacious.
Animal studies provide strong evidence for the involvement of the glutamatergic system in the expression of OCD-like behaviours.
A model incorporating both genetic and epigenetic mechanisms in the manifestation of OCD is suggested as a heuristic for the pathophysiology of OCD.
Obsessive–compulsive disorder has been scrutinized in many genetic, neuropsychological and neuroimaging studies. Pauls and colleagues provide an overview of our current understanding of the vulnerability factors, triggers and mechanisms underlying this devastating condition.
Obsessive–compulsive disorder (OCD) is characterized by repetitive thoughts and behaviours that are experienced as unwanted. Family and twin studies have demonstrated that OCD is a multifactorial familial condition that involves both polygenic and environmental risk factors. Neuroimaging studies have implicated the cortico–striato–thalamo–cortical circuit in the pathophysiology of the disorder, which is supported by the observation of specific neuropsychological impairments in patients with OCD, mainly in executive functions. Genetic studies indicate that genes affecting the serotonergic, dopaminergic and glutamatergic systems, and the interaction between them, play a crucial part in the functioning of this circuit. Environmental factors such as adverse perinatal events, psychological trauma and neurological trauma may modify the expression of risk genes and, hence, trigger the manifestation of obsessive–compulsive behaviours.</description><identifier>ISSN: 1471-003X</identifier><identifier>EISSN: 1471-0048</identifier><identifier>EISSN: 1469-3178</identifier><identifier>DOI: 10.1038/nrn3746</identifier><identifier>PMID: 24840803</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>45/43 ; 59/36 ; 631/1647/245/1627 ; 631/1647/245/1628 ; 631/208/205/2138 ; 692/699/476 ; Analysis ; Animal Genetics and Genomics ; Behavioral Sciences ; Biological Techniques ; Biomedicine ; Brain - pathology ; Development and progression ; Dopamine - metabolism ; Environment ; Family Health ; Genetic aspects ; Glutamic Acid - metabolism ; Humans ; Neural circuitry ; Neurobiology ; Neurosciences ; Obsessive compulsive disorder ; Obsessive-Compulsive Disorder - genetics ; Obsessive-Compulsive Disorder - pathology ; Obsessive-Compulsive Disorder - psychology ; Physiological aspects ; review-article ; Risk Factors ; Signal Transduction - physiology</subject><ispartof>Nature reviews. Neuroscience, 2014-06, Vol.15 (6), p.410-424</ispartof><rights>Springer Nature Limited 2014</rights><rights>COPYRIGHT 2014 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jun 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-198b22e59402e3dd2e5d45e359d62c100a284c794af67d673fb533155b8342ee3</citedby><cites>FETCH-LOGICAL-c442t-198b22e59402e3dd2e5d45e359d62c100a284c794af67d673fb533155b8342ee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24840803$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pauls, David L.</creatorcontrib><creatorcontrib>Abramovitch, Amitai</creatorcontrib><creatorcontrib>Rauch, Scott L.</creatorcontrib><creatorcontrib>Geller, Daniel A.</creatorcontrib><title>Obsessive–compulsive disorder: an integrative genetic and neurobiological perspective</title><title>Nature reviews. Neuroscience</title><addtitle>Nat Rev Neurosci</addtitle><addtitle>Nat Rev Neurosci</addtitle><description>Key Points
Obsessive–compulsive disorder (OCD) is a phenotypically complex multidimensional neuropsychiatric disorder.
Family and twin studies provide definitive evidence that genetic and environmental factors can increase risk of the disorder.
Candidate gene and genome-wide association studies provide strong suggestive evidence that genes in the serotonergic, dopaminergic and glutamatergic systems confer risk for the manifestation of OCD.
Imaging studies as well as neuropsychological and treatment studies have implicated frontal–subcortical circuits in the pathophysiology of OCD.
A cortico–striato–thalamo–cortical circuit is the prevailing model regarding the neural and pathophysiological underpinnings of OCD.
The prevailing treatments include both pharmacological agents (selective serotonin-reuptake inhibitors) and cognitive behavioural therapy (CBT), with CBT and/or a combination of pharmacological and CBT being the most efficacious.
Animal studies provide strong evidence for the involvement of the glutamatergic system in the expression of OCD-like behaviours.
A model incorporating both genetic and epigenetic mechanisms in the manifestation of OCD is suggested as a heuristic for the pathophysiology of OCD.
Obsessive–compulsive disorder has been scrutinized in many genetic, neuropsychological and neuroimaging studies. Pauls and colleagues provide an overview of our current understanding of the vulnerability factors, triggers and mechanisms underlying this devastating condition.
Obsessive–compulsive disorder (OCD) is characterized by repetitive thoughts and behaviours that are experienced as unwanted. Family and twin studies have demonstrated that OCD is a multifactorial familial condition that involves both polygenic and environmental risk factors. Neuroimaging studies have implicated the cortico–striato–thalamo–cortical circuit in the pathophysiology of the disorder, which is supported by the observation of specific neuropsychological impairments in patients with OCD, mainly in executive functions. Genetic studies indicate that genes affecting the serotonergic, dopaminergic and glutamatergic systems, and the interaction between them, play a crucial part in the functioning of this circuit. Environmental factors such as adverse perinatal events, psychological trauma and neurological trauma may modify the expression of risk genes and, hence, trigger the manifestation of obsessive–compulsive behaviours.</description><subject>45/43</subject><subject>59/36</subject><subject>631/1647/245/1627</subject><subject>631/1647/245/1628</subject><subject>631/208/205/2138</subject><subject>692/699/476</subject><subject>Analysis</subject><subject>Animal Genetics and Genomics</subject><subject>Behavioral Sciences</subject><subject>Biological Techniques</subject><subject>Biomedicine</subject><subject>Brain - pathology</subject><subject>Development and progression</subject><subject>Dopamine - metabolism</subject><subject>Environment</subject><subject>Family Health</subject><subject>Genetic aspects</subject><subject>Glutamic Acid - metabolism</subject><subject>Humans</subject><subject>Neural circuitry</subject><subject>Neurobiology</subject><subject>Neurosciences</subject><subject>Obsessive compulsive disorder</subject><subject>Obsessive-Compulsive Disorder - genetics</subject><subject>Obsessive-Compulsive Disorder - pathology</subject><subject>Obsessive-Compulsive Disorder - psychology</subject><subject>Physiological aspects</subject><subject>review-article</subject><subject>Risk Factors</subject><subject>Signal Transduction - physiology</subject><issn>1471-003X</issn><issn>1471-0048</issn><issn>1469-3178</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc1KHjEUhkNRqrXFO5ABF3Xzaf4mk3H3IdoWBDeVdhcyyZkhMpOMyYzgrvfgHXolZvCrVilZ5Pw85-UcXoT2CT4mmMkTHz2ruPiAdgmvyApjLrdeYvZ7B31K6QZjIkglPqIdyiXHErNd9OuqSZCSu4PHPw8mDOPcL0lhXQrRQjwttC-cn6CLeloaHXiYnMllW3iYY2hc6EPnjO6LEWIawSzcZ7Td6j7Bl82_h64vzn-efV9dXn37cba-XBnO6bQitWwohbLmmAKzNoeWl8DK2gpqCMaaSm6qmutWVFZUrG1KxkhZNpJxCsD20NGz7hjD7QxpUoNLBvpeewhzUqTMyoxyXGf08B16E-bo83aKCIGzuKTylep0D8r5NkxRm0VUrVmFGcWCskwd_4fKz8LgTPDQulx_M_D1ecDEkFKEVo3RDTreK4LVYqHaWJjJg82aczOAfeH-evZ6csot30H85453Wk9p0qM7</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>Pauls, David L.</creator><creator>Abramovitch, Amitai</creator><creator>Rauch, Scott L.</creator><creator>Geller, Daniel A.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20140601</creationdate><title>Obsessive–compulsive disorder: an integrative genetic and neurobiological perspective</title><author>Pauls, David L. ; Abramovitch, Amitai ; Rauch, Scott L. ; Geller, Daniel A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-198b22e59402e3dd2e5d45e359d62c100a284c794af67d673fb533155b8342ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>45/43</topic><topic>59/36</topic><topic>631/1647/245/1627</topic><topic>631/1647/245/1628</topic><topic>631/208/205/2138</topic><topic>692/699/476</topic><topic>Analysis</topic><topic>Animal Genetics and Genomics</topic><topic>Behavioral Sciences</topic><topic>Biological Techniques</topic><topic>Biomedicine</topic><topic>Brain - pathology</topic><topic>Development and progression</topic><topic>Dopamine - metabolism</topic><topic>Environment</topic><topic>Family Health</topic><topic>Genetic aspects</topic><topic>Glutamic Acid - metabolism</topic><topic>Humans</topic><topic>Neural circuitry</topic><topic>Neurobiology</topic><topic>Neurosciences</topic><topic>Obsessive compulsive disorder</topic><topic>Obsessive-Compulsive Disorder - genetics</topic><topic>Obsessive-Compulsive Disorder - pathology</topic><topic>Obsessive-Compulsive Disorder - psychology</topic><topic>Physiological aspects</topic><topic>review-article</topic><topic>Risk Factors</topic><topic>Signal Transduction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pauls, David L.</creatorcontrib><creatorcontrib>Abramovitch, Amitai</creatorcontrib><creatorcontrib>Rauch, Scott L.</creatorcontrib><creatorcontrib>Geller, Daniel A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Nature reviews. Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pauls, David L.</au><au>Abramovitch, Amitai</au><au>Rauch, Scott L.</au><au>Geller, Daniel A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Obsessive–compulsive disorder: an integrative genetic and neurobiological perspective</atitle><jtitle>Nature reviews. Neuroscience</jtitle><stitle>Nat Rev Neurosci</stitle><addtitle>Nat Rev Neurosci</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>15</volume><issue>6</issue><spage>410</spage><epage>424</epage><pages>410-424</pages><issn>1471-003X</issn><eissn>1471-0048</eissn><eissn>1469-3178</eissn><abstract>Key Points
Obsessive–compulsive disorder (OCD) is a phenotypically complex multidimensional neuropsychiatric disorder.
Family and twin studies provide definitive evidence that genetic and environmental factors can increase risk of the disorder.
Candidate gene and genome-wide association studies provide strong suggestive evidence that genes in the serotonergic, dopaminergic and glutamatergic systems confer risk for the manifestation of OCD.
Imaging studies as well as neuropsychological and treatment studies have implicated frontal–subcortical circuits in the pathophysiology of OCD.
A cortico–striato–thalamo–cortical circuit is the prevailing model regarding the neural and pathophysiological underpinnings of OCD.
The prevailing treatments include both pharmacological agents (selective serotonin-reuptake inhibitors) and cognitive behavioural therapy (CBT), with CBT and/or a combination of pharmacological and CBT being the most efficacious.
Animal studies provide strong evidence for the involvement of the glutamatergic system in the expression of OCD-like behaviours.
A model incorporating both genetic and epigenetic mechanisms in the manifestation of OCD is suggested as a heuristic for the pathophysiology of OCD.
Obsessive–compulsive disorder has been scrutinized in many genetic, neuropsychological and neuroimaging studies. Pauls and colleagues provide an overview of our current understanding of the vulnerability factors, triggers and mechanisms underlying this devastating condition.
Obsessive–compulsive disorder (OCD) is characterized by repetitive thoughts and behaviours that are experienced as unwanted. Family and twin studies have demonstrated that OCD is a multifactorial familial condition that involves both polygenic and environmental risk factors. Neuroimaging studies have implicated the cortico–striato–thalamo–cortical circuit in the pathophysiology of the disorder, which is supported by the observation of specific neuropsychological impairments in patients with OCD, mainly in executive functions. Genetic studies indicate that genes affecting the serotonergic, dopaminergic and glutamatergic systems, and the interaction between them, play a crucial part in the functioning of this circuit. Environmental factors such as adverse perinatal events, psychological trauma and neurological trauma may modify the expression of risk genes and, hence, trigger the manifestation of obsessive–compulsive behaviours.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24840803</pmid><doi>10.1038/nrn3746</doi><tpages>15</tpages></addata></record> |
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subjects | 45/43 59/36 631/1647/245/1627 631/1647/245/1628 631/208/205/2138 692/699/476 Analysis Animal Genetics and Genomics Behavioral Sciences Biological Techniques Biomedicine Brain - pathology Development and progression Dopamine - metabolism Environment Family Health Genetic aspects Glutamic Acid - metabolism Humans Neural circuitry Neurobiology Neurosciences Obsessive compulsive disorder Obsessive-Compulsive Disorder - genetics Obsessive-Compulsive Disorder - pathology Obsessive-Compulsive Disorder - psychology Physiological aspects review-article Risk Factors Signal Transduction - physiology |
title | Obsessive–compulsive disorder: an integrative genetic and neurobiological perspective |
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