Arlette F. Buchmann, Rainer Hellweg, Marcella Rietschel, Jens Treutlein, Stephanie H. Witt, Ulrich S. Zimmermann, Martin H. Schmidt, Günter Esser, Tobias Banaschewski, Manfred Laucht, Michael Deuschle
- Recent studies have emphasized an important role for neurotrophins, such as brain-derived neurotrophic factor (BDNF), in regulating the plasticity of neural circuits involved in the pathophysiology of stress-related diseases. The aim of the present study was to examine the interplay of the BDNF Val(66)Met and the serotonin transporter promoter (5-HTTLPR) polymorphisms in moderating the impact of early-life adversity on BDNF plasma concentration and depressive symptoms. Participants were taken from an epidemiological cohort study following the long-term outcome of early risk factors from birth into young adulthood. In 259 individuals (119 males, 140 females), genotyped for the BDNF Val(66)Met and the 5-HTTLPR polymorphisms, plasma BDNF was assessed at the age of 19 years. In addition, participants completed the Beck Depression Inventory (BDI). Early adversity was determined according to a family adversity index assessed at 3 months of age. Results indicated that individuals homozygous for both the BDNF Val and the 5-HTTLPR L alleleRecent studies have emphasized an important role for neurotrophins, such as brain-derived neurotrophic factor (BDNF), in regulating the plasticity of neural circuits involved in the pathophysiology of stress-related diseases. The aim of the present study was to examine the interplay of the BDNF Val(66)Met and the serotonin transporter promoter (5-HTTLPR) polymorphisms in moderating the impact of early-life adversity on BDNF plasma concentration and depressive symptoms. Participants were taken from an epidemiological cohort study following the long-term outcome of early risk factors from birth into young adulthood. In 259 individuals (119 males, 140 females), genotyped for the BDNF Val(66)Met and the 5-HTTLPR polymorphisms, plasma BDNF was assessed at the age of 19 years. In addition, participants completed the Beck Depression Inventory (BDI). Early adversity was determined according to a family adversity index assessed at 3 months of age. Results indicated that individuals homozygous for both the BDNF Val and the 5-HTTLPR L allele showed significantly reduced BDNF levels following exposure to high adversity. In contrast, BDNF levels appeared to be unaffected by early psychosocial adversity in carriers of the BDNF Met or the 5-HTTLPR S allele. While the former group appeared to be most susceptible to depressive symptoms, the impact of early adversity was less pronounced in the latter group. This is the first preliminary evidence indicating that early-life adverse experiences may have lasting sequelae for plasma BDNF levels in humans, highlighting that the susceptibility to this effect is moderated by BDNF Val(66)Met and 5-HTTLPR genotype.…
MetadatenVerfasserangaben: | Arlette F. Buchmann, Rainer Hellweg, Marcella Rietschel, Jens Treutlein, Stephanie H. Witt, Ulrich S. Zimmermann, Martin H. Schmidt, Günter EsserORCiDGND, Tobias BanaschewskiORCiD, Manfred LauchtGND, Michael DeuschleORCiDGND |
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DOI: | https://doi.org/10.1016/j.euroneuro.2012.09.003 |
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ISSN: | 0924-977X |
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Titel des übergeordneten Werks (Englisch): | European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology |
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Verlag: | Elsevier |
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Verlagsort: | Amsterdam |
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Publikationstyp: | Wissenschaftlicher Artikel |
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Sprache: | Englisch |
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Jahr der Erstveröffentlichung: | 2013 |
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Erscheinungsjahr: | 2013 |
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Datum der Freischaltung: | 26.03.2017 |
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Freies Schlagwort / Tag: | 5-HTTLPR; BDNF; Depression; Early psychosocial adversity; Human; Longitudinal study |
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Band: | 23 |
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Ausgabe: | 8 |
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Seitenanzahl: | 8 |
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Erste Seite: | 902 |
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Letzte Seite: | 909 |
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Fördernde Institution: | German Research Foundation (DFG); Federal Ministry for Education and
Research as part of the 'Baden-Wuerttemberg Consortium for Addiction
Research'; National Genome Research Network |
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Organisationseinheiten: | Humanwissenschaftliche Fakultät / Strukturbereich Kognitionswissenschaften / Department Psychologie |
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Peer Review: | Referiert |
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Name der Einrichtung zum Zeitpunkt der Publikation: | Humanwissenschaftliche Fakultät / Institut für Psychologie |
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