Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia
▶ This review details how putative schizophrenia risk genes regulate neuroplasticity. ▶ Highlights how risk genes converge to regulate common neurotransmitter systems. ▶ Highlights how risk genes converge on common signaling pathways. Schizophrenia is a severe mental illness that afflicts nearly 1%...
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| Veröffentlicht in: | Neuroscience and biobehavioral reviews 2011-01, Vol.35 (3), p.848-870 |
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| creator | Balu, Darrick T. Coyle, Joseph T. |
| description | ▶ This review details how putative schizophrenia risk genes regulate neuroplasticity. ▶ Highlights how risk genes converge to regulate common neurotransmitter systems. ▶ Highlights how risk genes converge on common signaling pathways.
Schizophrenia is a severe mental illness that afflicts nearly 1% of the world's population. One of the cardinal pathological features of schizophrenia is perturbation in synaptic connectivity. Although the etiology of schizophrenia is unknown, it appears to be a developmental disorder involving the interaction of a potentially large number of risk genes, with no one gene producing a strong effect except rare, highly penetrant copy number variants. The purpose of this review is to detail how putative schizophrenia risk genes (DISC-1, neuregulin/ErbB4, dysbindin, Akt1, BDNF, and the NMDA receptor) are involved in regulating neuroplasticity and how alterations in their expression may contribute to the disconnectivity observed in schizophrenia. Moreover, this review highlights how many of these risk genes converge to regulate common neurotransmitter systems and signaling pathways. Future studies aimed at elucidating the functions of these risk genes will provide new insights into the pathophysiology of schizophrenia and will likely lead to the nomination of novel therapeutic targets for restoring proper synaptic connectivity in the brain in schizophrenia and related disorders. |
| doi_str_mv | 10.1016/j.neubiorev.2010.10.005 |
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Schizophrenia is a severe mental illness that afflicts nearly 1% of the world's population. One of the cardinal pathological features of schizophrenia is perturbation in synaptic connectivity. Although the etiology of schizophrenia is unknown, it appears to be a developmental disorder involving the interaction of a potentially large number of risk genes, with no one gene producing a strong effect except rare, highly penetrant copy number variants. The purpose of this review is to detail how putative schizophrenia risk genes (DISC-1, neuregulin/ErbB4, dysbindin, Akt1, BDNF, and the NMDA receptor) are involved in regulating neuroplasticity and how alterations in their expression may contribute to the disconnectivity observed in schizophrenia. Moreover, this review highlights how many of these risk genes converge to regulate common neurotransmitter systems and signaling pathways. Future studies aimed at elucidating the functions of these risk genes will provide new insights into the pathophysiology of schizophrenia and will likely lead to the nomination of novel therapeutic targets for restoring proper synaptic connectivity in the brain in schizophrenia and related disorders.</description><identifier>ISSN: 0149-7634</identifier><identifier>EISSN: 1873-7528</identifier><identifier>DOI: 10.1016/j.neubiorev.2010.10.005</identifier><identifier>PMID: 20951727</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>Adult and adolescent clinical studies ; Akt1 ; Animals ; BDNF ; Behavioral psychophysiology ; Biological and medical sciences ; DISC-1 ; Dysbindin ; ErbB4 ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - physiology ; Humans ; Medical sciences ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Neuregulin ; Neuronal Plasticity - physiology ; NMDA receptor ; Psychology. Psychoanalysis. Psychiatry ; Psychology. Psychophysiology ; Psychopathology. Psychiatry ; Psychoses ; Schizophrenia ; Schizophrenia - physiopathology ; Signal Transduction - physiology</subject><ispartof>Neuroscience and biobehavioral reviews, 2011-01, Vol.35 (3), p.848-870</ispartof><rights>2010</rights><rights>2015 INIST-CNRS</rights><rights>Published by Elsevier Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c602t-54329c985f48ef8e19bc79b35c4ceb834d9d80a782926418e142d7e2162633353</citedby><cites>FETCH-LOGICAL-c602t-54329c985f48ef8e19bc79b35c4ceb834d9d80a782926418e142d7e2162633353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neubiorev.2010.10.005$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23838778$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20951727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Balu, Darrick T.</creatorcontrib><creatorcontrib>Coyle, Joseph T.</creatorcontrib><title>Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia</title><title>Neuroscience and biobehavioral reviews</title><addtitle>Neurosci Biobehav Rev</addtitle><description>▶ This review details how putative schizophrenia risk genes regulate neuroplasticity. ▶ Highlights how risk genes converge to regulate common neurotransmitter systems. ▶ Highlights how risk genes converge on common signaling pathways.
Schizophrenia is a severe mental illness that afflicts nearly 1% of the world's population. One of the cardinal pathological features of schizophrenia is perturbation in synaptic connectivity. Although the etiology of schizophrenia is unknown, it appears to be a developmental disorder involving the interaction of a potentially large number of risk genes, with no one gene producing a strong effect except rare, highly penetrant copy number variants. The purpose of this review is to detail how putative schizophrenia risk genes (DISC-1, neuregulin/ErbB4, dysbindin, Akt1, BDNF, and the NMDA receptor) are involved in regulating neuroplasticity and how alterations in their expression may contribute to the disconnectivity observed in schizophrenia. Moreover, this review highlights how many of these risk genes converge to regulate common neurotransmitter systems and signaling pathways. Future studies aimed at elucidating the functions of these risk genes will provide new insights into the pathophysiology of schizophrenia and will likely lead to the nomination of novel therapeutic targets for restoring proper synaptic connectivity in the brain in schizophrenia and related disorders.</description><subject>Adult and adolescent clinical studies</subject><subject>Akt1</subject><subject>Animals</subject><subject>BDNF</subject><subject>Behavioral psychophysiology</subject><subject>Biological and medical sciences</subject><subject>DISC-1</subject><subject>Dysbindin</subject><subject>ErbB4</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - physiology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neuregulin</subject><subject>Neuronal Plasticity - physiology</subject><subject>NMDA receptor</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. Psychophysiology</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychoses</subject><subject>Schizophrenia</subject><subject>Schizophrenia - physiopathology</subject><subject>Signal Transduction - physiology</subject><issn>0149-7634</issn><issn>1873-7528</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU-P0zAQxS0EYsvCV4BcEKcU_4lj-4K0WrGAtAIhwdlynEnjksbBdorCp193Wwqc4GT5zW9Gb-Yh9ILgNcGkfr1djzA3zgfYrym-V9cY8wdoRaRgpeBUPkQrTCpVippVF-hJjFuMMcWMP0YXFCtOBBUr9PkjzMFPg4nJWZeWIrrNaAY3borJpP6HWWKRf9-gLZIvUg_3sp_6JTo_-M1S-K6Itnc_sxZgdOYpetSZIcKz03uJvt68_XL9vrz99O7D9dVtaWtMU8krRpVVkneVhE4CUY0VqmHcVhYayapWtRIbIamidUUyUNFWACU1rRljnF2iN8e509zsoLUwpmAGPQW3M2HR3jj9d2V0vd74vWb5UJKyPODVaUDw32eISe9ctDAMZgQ_Ry1rxSVX4j9ISogilMtMiiNpg48xQHf2Q7A-JKe3-pycPiR3KGRDufP5n-uc-35FlYGXJ8BEa4YumNG6-JtjkkkhDhaujhzk4-8dBB2tg9FC6wLYpFvv_mnmDjAvvVk</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Balu, Darrick T.</creator><creator>Coyle, Joseph T.</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope><scope>7QG</scope><scope>7TK</scope><scope>5PM</scope></search><sort><creationdate>20110101</creationdate><title>Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia</title><author>Balu, Darrick T. ; Coyle, Joseph T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c602t-54329c985f48ef8e19bc79b35c4ceb834d9d80a782926418e142d7e2162633353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult and adolescent clinical studies</topic><topic>Akt1</topic><topic>Animals</topic><topic>BDNF</topic><topic>Behavioral psychophysiology</topic><topic>Biological and medical sciences</topic><topic>DISC-1</topic><topic>Dysbindin</topic><topic>ErbB4</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - physiology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neuregulin</topic><topic>Neuronal Plasticity - physiology</topic><topic>NMDA receptor</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychology. Psychophysiology</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychoses</topic><topic>Schizophrenia</topic><topic>Schizophrenia - physiopathology</topic><topic>Signal Transduction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Balu, Darrick T.</creatorcontrib><creatorcontrib>Coyle, Joseph T.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuroscience and biobehavioral reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Balu, Darrick T.</au><au>Coyle, Joseph T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia</atitle><jtitle>Neuroscience and biobehavioral reviews</jtitle><addtitle>Neurosci Biobehav Rev</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>35</volume><issue>3</issue><spage>848</spage><epage>870</epage><pages>848-870</pages><issn>0149-7634</issn><eissn>1873-7528</eissn><abstract>▶ This review details how putative schizophrenia risk genes regulate neuroplasticity. ▶ Highlights how risk genes converge to regulate common neurotransmitter systems. ▶ Highlights how risk genes converge on common signaling pathways.
Schizophrenia is a severe mental illness that afflicts nearly 1% of the world's population. One of the cardinal pathological features of schizophrenia is perturbation in synaptic connectivity. Although the etiology of schizophrenia is unknown, it appears to be a developmental disorder involving the interaction of a potentially large number of risk genes, with no one gene producing a strong effect except rare, highly penetrant copy number variants. The purpose of this review is to detail how putative schizophrenia risk genes (DISC-1, neuregulin/ErbB4, dysbindin, Akt1, BDNF, and the NMDA receptor) are involved in regulating neuroplasticity and how alterations in their expression may contribute to the disconnectivity observed in schizophrenia. Moreover, this review highlights how many of these risk genes converge to regulate common neurotransmitter systems and signaling pathways. Future studies aimed at elucidating the functions of these risk genes will provide new insights into the pathophysiology of schizophrenia and will likely lead to the nomination of novel therapeutic targets for restoring proper synaptic connectivity in the brain in schizophrenia and related disorders.</abstract><cop>Kidlington</cop><pub>Elsevier Ltd</pub><pmid>20951727</pmid><doi>10.1016/j.neubiorev.2010.10.005</doi><tpages>23</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult and adolescent clinical studies Akt1 Animals BDNF Behavioral psychophysiology Biological and medical sciences DISC-1 Dysbindin ErbB4 Fundamental and applied biological sciences. Psychology Gene Expression Regulation - physiology Humans Medical sciences Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Neuregulin Neuronal Plasticity - physiology NMDA receptor Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Psychopathology. Psychiatry Psychoses Schizophrenia Schizophrenia - physiopathology Signal Transduction - physiology |
| title | Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia |
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