Interplay of Val66Met and BDNF methylation: effect on reward learning and cognitive performance in major depression
There is a growing interest in the role of brain-derived neurotrophic factor (BDNF) in major depressive disorder (MDD). BDNF potentially exhibits opposite effects in the pathways linked to anhedonia and reward learning on the one hand and cognitive performance, on the other hand. However, the epigen...
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description | There is a growing interest in the role of brain-derived neurotrophic factor (BDNF) in major depressive disorder (MDD). BDNF potentially exhibits opposite effects in the pathways linked to anhedonia and reward learning on the one hand and cognitive performance, on the other hand. However, the epigenetic mechanisms behind this remain unknown. In the present study, we aimed to investigate the interplay of DNA methylation of different BDNF exons and the common Val66Met polymorphism on anhedonia, reward learning and cognitive performance in MDD.
We recruited 80 depressed patients and 58 age- and gender-matched healthy controls. Participants underwent clinical assessment including neuropsychological testing and a probabilistic reward task to assess reward learning. Val66Met polymorphism and DNA methylation of BDNF promoters I, IV and exon IX were assessed from whole blood derived DNA, using pyrosequencing.
BDNF promoter I methylation was lower in MDD patients (p = 0.042) and was negatively associated with self-reported anhedonia. In depressed patients, both Val66Met polymorphism and DNA methylation of promoter I were significantly associated with reward bias (p |
doi_str_mv | 10.1186/s13148-021-01136-z |
format | Article |
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We recruited 80 depressed patients and 58 age- and gender-matched healthy controls. Participants underwent clinical assessment including neuropsychological testing and a probabilistic reward task to assess reward learning. Val66Met polymorphism and DNA methylation of BDNF promoters I, IV and exon IX were assessed from whole blood derived DNA, using pyrosequencing.
BDNF promoter I methylation was lower in MDD patients (p = 0.042) and was negatively associated with self-reported anhedonia. In depressed patients, both Val66Met polymorphism and DNA methylation of promoter I were significantly associated with reward bias (p < 0.050 and p = 0.040, respectively), without an interaction effect. On the other hand, methylation of exon IX had a negative impact on executive functioning (p = 0.002) and mediated the effect of Val66Met on this outcome in patients with MDD.
Our results provide the first evidence of Val66Met susceptibility to differential epigenetic regulation of BDNF exons in reward learning and executive functioning in MDD, which needs to be further explored.</description><identifier>ISSN: 1868-7075</identifier><identifier>ISSN: 1868-7083</identifier><identifier>EISSN: 1868-7083</identifier><identifier>EISSN: 1868-7075</identifier><identifier>DOI: 10.1186/s13148-021-01136-z</identifier><identifier>PMID: 34325733</identifier><language>eng</language><publisher>Germany: BioMed Central Ltd</publisher><subject>Adult ; Belgium ; Brain research ; Brain-derived neurotrophic factor ; Brain-Derived Neurotrophic Factor - analysis ; Brain-Derived Neurotrophic Factor - genetics ; Cognition ; Cognitive ability ; Deoxyribonucleic acid ; Depressive Disorder, Major - epidemiology ; Depressive Disorder, Major - genetics ; DNA ; DNA methylation ; DNA Methylation - genetics ; DNA Methylation - physiology ; Epigenetic inheritance ; Epigenetics ; Executive function ; Exons ; Female ; Genetic polymorphisms ; Genetic testing ; Hedonic response ; Humans ; Hypotheses ; Learning ; Major depressive disorder ; Male ; Measuring techniques ; Mental depression ; Methylation ; Middle Aged ; Neuropsychology ; Patients ; Polymorphism ; Psychology ; Psychometrics - instrumentation ; Psychometrics - methods ; Reinforcement</subject><ispartof>Clinical epigenetics, 2021-12, Vol.13 (1), p.149-149, Article 149</ispartof><rights>2021. The Author(s).</rights><rights>COPYRIGHT 2021 BioMed Central Ltd.</rights><rights>2021. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c497t-d80dcc70b53c2d02494ecb65cb89d2a354eaf347f7c70203ba956a47b3549203</citedby><cites>FETCH-LOGICAL-c497t-d80dcc70b53c2d02494ecb65cb89d2a354eaf347f7c70203ba956a47b3549203</cites><orcidid>0000-0002-0953-6974</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8323304/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8323304/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34325733$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bakusic, J</creatorcontrib><creatorcontrib>Vrieze, E</creatorcontrib><creatorcontrib>Ghosh, M</creatorcontrib><creatorcontrib>Pizzagalli, D A</creatorcontrib><creatorcontrib>Bekaert, B</creatorcontrib><creatorcontrib>Claes, S</creatorcontrib><creatorcontrib>Godderis, L</creatorcontrib><title>Interplay of Val66Met and BDNF methylation: effect on reward learning and cognitive performance in major depression</title><title>Clinical epigenetics</title><addtitle>Clin Epigenetics</addtitle><description>There is a growing interest in the role of brain-derived neurotrophic factor (BDNF) in major depressive disorder (MDD). BDNF potentially exhibits opposite effects in the pathways linked to anhedonia and reward learning on the one hand and cognitive performance, on the other hand. However, the epigenetic mechanisms behind this remain unknown. In the present study, we aimed to investigate the interplay of DNA methylation of different BDNF exons and the common Val66Met polymorphism on anhedonia, reward learning and cognitive performance in MDD.
We recruited 80 depressed patients and 58 age- and gender-matched healthy controls. Participants underwent clinical assessment including neuropsychological testing and a probabilistic reward task to assess reward learning. Val66Met polymorphism and DNA methylation of BDNF promoters I, IV and exon IX were assessed from whole blood derived DNA, using pyrosequencing.
BDNF promoter I methylation was lower in MDD patients (p = 0.042) and was negatively associated with self-reported anhedonia. In depressed patients, both Val66Met polymorphism and DNA methylation of promoter I were significantly associated with reward bias (p < 0.050 and p = 0.040, respectively), without an interaction effect. On the other hand, methylation of exon IX had a negative impact on executive functioning (p = 0.002) and mediated the effect of Val66Met on this outcome in patients with MDD.
Our results provide the first evidence of Val66Met susceptibility to differential epigenetic regulation of BDNF exons in reward learning and executive functioning in MDD, which needs to be further explored.</description><subject>Adult</subject><subject>Belgium</subject><subject>Brain research</subject><subject>Brain-derived neurotrophic factor</subject><subject>Brain-Derived Neurotrophic Factor - analysis</subject><subject>Brain-Derived Neurotrophic Factor - genetics</subject><subject>Cognition</subject><subject>Cognitive ability</subject><subject>Deoxyribonucleic acid</subject><subject>Depressive Disorder, Major - epidemiology</subject><subject>Depressive Disorder, Major - genetics</subject><subject>DNA</subject><subject>DNA methylation</subject><subject>DNA Methylation - genetics</subject><subject>DNA Methylation - physiology</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>Executive function</subject><subject>Exons</subject><subject>Female</subject><subject>Genetic polymorphisms</subject><subject>Genetic testing</subject><subject>Hedonic response</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Learning</subject><subject>Major depressive disorder</subject><subject>Male</subject><subject>Measuring techniques</subject><subject>Mental depression</subject><subject>Methylation</subject><subject>Middle Aged</subject><subject>Neuropsychology</subject><subject>Patients</subject><subject>Polymorphism</subject><subject>Psychology</subject><subject>Psychometrics - 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analysis</topic><topic>Brain-Derived Neurotrophic Factor - genetics</topic><topic>Cognition</topic><topic>Cognitive ability</topic><topic>Deoxyribonucleic acid</topic><topic>Depressive Disorder, Major - epidemiology</topic><topic>Depressive Disorder, Major - genetics</topic><topic>DNA</topic><topic>DNA methylation</topic><topic>DNA Methylation - genetics</topic><topic>DNA Methylation - physiology</topic><topic>Epigenetic inheritance</topic><topic>Epigenetics</topic><topic>Executive function</topic><topic>Exons</topic><topic>Female</topic><topic>Genetic polymorphisms</topic><topic>Genetic testing</topic><topic>Hedonic response</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Learning</topic><topic>Major depressive disorder</topic><topic>Male</topic><topic>Measuring techniques</topic><topic>Mental depression</topic><topic>Methylation</topic><topic>Middle Aged</topic><topic>Neuropsychology</topic><topic>Patients</topic><topic>Polymorphism</topic><topic>Psychology</topic><topic>Psychometrics - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical epigenetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bakusic, J</au><au>Vrieze, E</au><au>Ghosh, M</au><au>Pizzagalli, D A</au><au>Bekaert, B</au><au>Claes, S</au><au>Godderis, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interplay of Val66Met and BDNF methylation: effect on reward learning and cognitive performance in major depression</atitle><jtitle>Clinical epigenetics</jtitle><addtitle>Clin Epigenetics</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>13</volume><issue>1</issue><spage>149</spage><epage>149</epage><pages>149-149</pages><artnum>149</artnum><issn>1868-7075</issn><issn>1868-7083</issn><eissn>1868-7083</eissn><eissn>1868-7075</eissn><abstract>There is a growing interest in the role of brain-derived neurotrophic factor (BDNF) in major depressive disorder (MDD). BDNF potentially exhibits opposite effects in the pathways linked to anhedonia and reward learning on the one hand and cognitive performance, on the other hand. However, the epigenetic mechanisms behind this remain unknown. In the present study, we aimed to investigate the interplay of DNA methylation of different BDNF exons and the common Val66Met polymorphism on anhedonia, reward learning and cognitive performance in MDD.
We recruited 80 depressed patients and 58 age- and gender-matched healthy controls. Participants underwent clinical assessment including neuropsychological testing and a probabilistic reward task to assess reward learning. Val66Met polymorphism and DNA methylation of BDNF promoters I, IV and exon IX were assessed from whole blood derived DNA, using pyrosequencing.
BDNF promoter I methylation was lower in MDD patients (p = 0.042) and was negatively associated with self-reported anhedonia. In depressed patients, both Val66Met polymorphism and DNA methylation of promoter I were significantly associated with reward bias (p < 0.050 and p = 0.040, respectively), without an interaction effect. On the other hand, methylation of exon IX had a negative impact on executive functioning (p = 0.002) and mediated the effect of Val66Met on this outcome in patients with MDD.
Our results provide the first evidence of Val66Met susceptibility to differential epigenetic regulation of BDNF exons in reward learning and executive functioning in MDD, which needs to be further explored.</abstract><cop>Germany</cop><pub>BioMed Central Ltd</pub><pmid>34325733</pmid><doi>10.1186/s13148-021-01136-z</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-0953-6974</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adult Belgium Brain research Brain-derived neurotrophic factor Brain-Derived Neurotrophic Factor - analysis Brain-Derived Neurotrophic Factor - genetics Cognition Cognitive ability Deoxyribonucleic acid Depressive Disorder, Major - epidemiology Depressive Disorder, Major - genetics DNA DNA methylation DNA Methylation - genetics DNA Methylation - physiology Epigenetic inheritance Epigenetics Executive function Exons Female Genetic polymorphisms Genetic testing Hedonic response Humans Hypotheses Learning Major depressive disorder Male Measuring techniques Mental depression Methylation Middle Aged Neuropsychology Patients Polymorphism Psychology Psychometrics - instrumentation Psychometrics - methods Reinforcement |
title | Interplay of Val66Met and BDNF methylation: effect on reward learning and cognitive performance in major depression |
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