Is it time to reassess the BDNF hypothesis of depression?
The brain-derived neurotrophic factor (BDNF) hypothesis of depression postulates that a loss of BDNF is directly involved in the pathophysiology of depression, and that its restoration may underlie the therapeutic efficacy of antidepressant treatment. While this theory has received considerable expe...
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| Veröffentlicht in: | Molecular psychiatry 2007-12, Vol.12 (12), p.1079-1088 |
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| description | The brain-derived neurotrophic factor (BDNF) hypothesis of depression postulates that a loss of BDNF is directly involved in the pathophysiology of depression, and that its restoration may underlie the therapeutic efficacy of antidepressant treatment. While this theory has received considerable experimental support, an increasing number of studies have generated evidence which is not only inconsistent, but also directly contradicts the hypothesis. This article provides a critical review of the clinical and preclinical studies which have been responsible for this controversy, outlining pharmacological, behavioural and genetic evidence which demonstrates the contrasting role of BDNF in regulating mood and antidepressant effects throughout the brain. I will also review key studies, both human and animal, which have investigated the association of a BDNF single-nucleotide polymorphism (Val66Met) with depression pathogenesis, and detail the number of inconsistencies which also afflict this novel area of BDNF research. The article will conclude by discussing why now is a critical time to reassess the original BDNF hypothesis of depression, and look towards the formation of new models that can provide a more valid account of the complex relationships between growth factors, mood disorders and their treatment. |
| doi_str_mv | 10.1038/sj.mp.4002075 |
| format | Article |
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While this theory has received considerable experimental support, an increasing number of studies have generated evidence which is not only inconsistent, but also directly contradicts the hypothesis. This article provides a critical review of the clinical and preclinical studies which have been responsible for this controversy, outlining pharmacological, behavioural and genetic evidence which demonstrates the contrasting role of BDNF in regulating mood and antidepressant effects throughout the brain. I will also review key studies, both human and animal, which have investigated the association of a BDNF single-nucleotide polymorphism (Val66Met) with depression pathogenesis, and detail the number of inconsistencies which also afflict this novel area of BDNF research. The article will conclude by discussing why now is a critical time to reassess the original BDNF hypothesis of depression, and look towards the formation of new models that can provide a more valid account of the complex relationships between growth factors, mood disorders and their treatment.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/sj.mp.4002075</identifier><identifier>PMID: 17700574</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adult and adolescent clinical studies ; Animals ; Antidepressants ; Behavioral Sciences ; Biological and medical sciences ; Biological Psychology ; Brain research ; Brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor - genetics ; Brain-Derived Neurotrophic Factor - metabolism ; Cell growth ; Depression ; Depression - genetics ; Depression - metabolism ; Depression - physiopathology ; Depression, Mental ; Development and progression ; Evaluation ; feature-review ; Genetic aspects ; Growth factors ; Health aspects ; Humans ; Hypotheses ; Kinases ; Medical sciences ; Medicine ; Medicine & Public Health ; Mental depression ; Methionine - genetics ; Models, Biological ; Mood ; Mood disorders ; Neurogenesis ; Neuropharmacology ; Neurosciences ; Pathogenesis ; Pathophysiology ; Pharmacology. Drug treatments ; Pharmacotherapy ; Polymorphism, Single Nucleotide - genetics ; Properties ; Proteins ; Psychiatry ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. 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While this theory has received considerable experimental support, an increasing number of studies have generated evidence which is not only inconsistent, but also directly contradicts the hypothesis. This article provides a critical review of the clinical and preclinical studies which have been responsible for this controversy, outlining pharmacological, behavioural and genetic evidence which demonstrates the contrasting role of BDNF in regulating mood and antidepressant effects throughout the brain. I will also review key studies, both human and animal, which have investigated the association of a BDNF single-nucleotide polymorphism (Val66Met) with depression pathogenesis, and detail the number of inconsistencies which also afflict this novel area of BDNF research. The article will conclude by discussing why now is a critical time to reassess the original BDNF hypothesis of depression, and look towards the formation of new models that can provide a more valid account of the complex relationships between growth factors, mood disorders and their treatment.</description><subject>Adult and adolescent clinical studies</subject><subject>Animals</subject><subject>Antidepressants</subject><subject>Behavioral Sciences</subject><subject>Biological and medical sciences</subject><subject>Biological Psychology</subject><subject>Brain research</subject><subject>Brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor - genetics</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Cell growth</subject><subject>Depression</subject><subject>Depression - genetics</subject><subject>Depression - metabolism</subject><subject>Depression - physiopathology</subject><subject>Depression, Mental</subject><subject>Development and progression</subject><subject>Evaluation</subject><subject>feature-review</subject><subject>Genetic aspects</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Kinases</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mental depression</subject><subject>Methionine - genetics</subject><subject>Models, Biological</subject><subject>Mood</subject><subject>Mood disorders</subject><subject>Neurogenesis</subject><subject>Neuropharmacology</subject><subject>Neurosciences</subject><subject>Pathogenesis</subject><subject>Pathophysiology</subject><subject>Pharmacology. Drug treatments</subject><subject>Pharmacotherapy</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Properties</subject><subject>Proteins</subject><subject>Psychiatry</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychopharmacology</subject><subject>Risk factors</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Valine - genetics</subject><issn>1359-4184</issn><issn>1476-5578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</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>eNqFkk1v1DAQhiMEoqVw5IoiEHDKMk7seHyqSqFQqYJL75bXsVuvkjh4sof-exw1YgUqIB_88T4z74w1RfGSwYZBgx9otxmmDQeoQYpHxTHjsq2EkPg4nxuhKs6QHxXPiHYAiyieFkdMSgAh-XGhLqkMczmHwZVzLJMzRI6onG9d-fHTt4vy9m6K-UKByujLzk0pyyGOp8-LJ9705F6s-0lxffH5-vxrdfX9y-X52VVlBfK5cjWKzivFbW07QIFolEHOO8EQlbNbQIUWOo6qYw6Y4l6Cr7ccTQ1cNCfF-_u0U4o_9o5mPQSyru_N6OKetBSqYaJtFvLdP8kWBcdGqv-C2ZchNDKDb_4Ad3GfxtytrlsuZNuCWqjXf6VqVjdN26pDqhvTOx1GH-dk7OKrz5gCJhgXLFObB6i8OjcEG0fnQ37_LaC6D7ApEiXn9ZTCYNKdZqCX-dC008Ok1_nI_Ku11v12cN2BXgciA29XwJA1vU9mtIEOnEJZt_m7f1VKWRpvXDo0_bDzT3MyzI4</recordid><startdate>20071201</startdate><enddate>20071201</enddate><creator>Groves, J O</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20071201</creationdate><title>Is it time to reassess the BDNF hypothesis of depression?</title><author>Groves, J O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c584t-e285df994c2cd08588a9a844d51889ecb0898c0d489d1e0194f70f2b48a20453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult and adolescent clinical studies</topic><topic>Animals</topic><topic>Antidepressants</topic><topic>Behavioral Sciences</topic><topic>Biological and medical sciences</topic><topic>Biological Psychology</topic><topic>Brain research</topic><topic>Brain-derived neurotrophic factor</topic><topic>Brain-Derived Neurotrophic Factor - genetics</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Cell growth</topic><topic>Depression</topic><topic>Depression - genetics</topic><topic>Depression - metabolism</topic><topic>Depression - physiopathology</topic><topic>Depression, Mental</topic><topic>Development and progression</topic><topic>Evaluation</topic><topic>feature-review</topic><topic>Genetic aspects</topic><topic>Growth factors</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Kinases</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mental depression</topic><topic>Methionine - genetics</topic><topic>Models, Biological</topic><topic>Mood</topic><topic>Mood disorders</topic><topic>Neurogenesis</topic><topic>Neuropharmacology</topic><topic>Neurosciences</topic><topic>Pathogenesis</topic><topic>Pathophysiology</topic><topic>Pharmacology. Drug treatments</topic><topic>Pharmacotherapy</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Properties</topic><topic>Proteins</topic><topic>Psychiatry</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Risk factors</topic><topic>Single nucleotide polymorphisms</topic><topic>Single-nucleotide polymorphism</topic><topic>Valine - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Groves, J O</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>ProQuest Central (Corporate)</collection><collection>Neurosciences 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>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>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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Groves, J O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Is it time to reassess the BDNF hypothesis of depression?</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>2007-12-01</date><risdate>2007</risdate><volume>12</volume><issue>12</issue><spage>1079</spage><epage>1088</epage><pages>1079-1088</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><abstract>The brain-derived neurotrophic factor (BDNF) hypothesis of depression postulates that a loss of BDNF is directly involved in the pathophysiology of depression, and that its restoration may underlie the therapeutic efficacy of antidepressant treatment. While this theory has received considerable experimental support, an increasing number of studies have generated evidence which is not only inconsistent, but also directly contradicts the hypothesis. This article provides a critical review of the clinical and preclinical studies which have been responsible for this controversy, outlining pharmacological, behavioural and genetic evidence which demonstrates the contrasting role of BDNF in regulating mood and antidepressant effects throughout the brain. I will also review key studies, both human and animal, which have investigated the association of a BDNF single-nucleotide polymorphism (Val66Met) with depression pathogenesis, and detail the number of inconsistencies which also afflict this novel area of BDNF research. The article will conclude by discussing why now is a critical time to reassess the original BDNF hypothesis of depression, and look towards the formation of new models that can provide a more valid account of the complex relationships between growth factors, mood disorders and their treatment.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>17700574</pmid><doi>10.1038/sj.mp.4002075</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult and adolescent clinical studies Animals Antidepressants Behavioral Sciences Biological and medical sciences Biological Psychology Brain research Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - genetics Brain-Derived Neurotrophic Factor - metabolism Cell growth Depression Depression - genetics Depression - metabolism Depression - physiopathology Depression, Mental Development and progression Evaluation feature-review Genetic aspects Growth factors Health aspects Humans Hypotheses Kinases Medical sciences Medicine Medicine & Public Health Mental depression Methionine - genetics Models, Biological Mood Mood disorders Neurogenesis Neuropharmacology Neurosciences Pathogenesis Pathophysiology Pharmacology. Drug treatments Pharmacotherapy Polymorphism, Single Nucleotide - genetics Properties Proteins Psychiatry Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychopharmacology Risk factors Single nucleotide polymorphisms Single-nucleotide polymorphism Valine - genetics |
| title | Is it time to reassess the BDNF hypothesis of depression? |
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