PMID- 30078664 OWN - NLM STAT- MEDLINE DCOM- 20190227 LR - 20190322 IS - 1573-2517 (Electronic) IS - 0165-0327 (Linking) VI - 243 DP - 2019 Jan 15 TI - The impact of BDNF Val66Met polymorphism on cognition in Bipolar Disorder: A review: Special Section on "Translational and Neuroscience Studies in Affective Disorders" Section Editor, Maria Nobile MD, PhD. This Section of JAD focuses on the relevance of translational and neuroscience studies in providing a better understanding of the neural basis of affective disorders. The main aim is to briefly summaries relevant research findings in clinical neuroscience with particular regards to specific innovative topics in mood and anxiety disorders. PG - 552-558 LID - S0165-0327(18)30909-1 [pii] LID - 10.1016/j.jad.2018.07.054 [doi] AB - BACKGROUND: Converging lines of evidence suggest that Brain-Derived Neurotrophic Factor (BDNF) may play a central role in the pathogenesis of Bipolar Disorder (BD), thus representing a valid biomarker of the disease. A common genetic variation in the BDNF gene, the Val66Met, is associated with reduced maturation and secretion of BDNF and therefore it has been related to specific mood, cognitive and neuroanatomical alterations in BD. However, so far, only a handful of studies have investigated the association between Val66Met polymorphism and cognitive functioning in BD. METHODS: We performed a bibliographic search on PUBMED of all genetic studies investigating Val66Met modulation on cognitive performances in BD subjects. The inclusion criteria were met by nine studies, including a total amount of 897 BD subjects and 803 healthy controls. RESULTS: From the analysis of the existing literature emerged that a) Val allele in BD adults, but not in BD adolescents, was associated with better performances in selective cognitive domains including executive functions, verbal learning and memory; b) Met allele may negatively modulate the association between childhood trauma and performances in memory, verbal ability and verbal fluency tasks; c) Met allele may also negatively regulate structural abnormalities in cognitive cerebral structures; d) Val/Met carriers showed greater improvements in cognitive functions compared to Val/Val and Met/Met carriers. LIMITATIONS: Few genetic studies exploring the impact of Val66Met on cognition in BD. CONCLUSIONS: Val66Met polymorphism likely modulates cognitive functions in BD patients with complex gene-environment interactions and through potential modulations of cerebral structures. Further and larger genetic studies are required in order to detect association between BDNF polymorphism, BDNF levels, brain abnormalities and cognition in BD. CI - Copyright (c) 2018 Elsevier B.V. All rights reserved. FAU - Mandolini, G M AU - Mandolini GM AD - Department of Neurosciences and Mental Health, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy. Electronic address: gianmario.mandolini@gmail.com. FAU - Lazzaretti, M AU - Lazzaretti M AD - Department of Neurosciences and Mental Health, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy. FAU - Pigoni, A AU - Pigoni A AD - Department of Neurosciences and Mental Health, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy. FAU - Delvecchio, G AU - Delvecchio G AD - Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy. FAU - Soares, J C AU - Soares JC AD - Department of Psychiatry and Behavioural Neurosciences, University of Texas, Houston, TX, USA. FAU - Brambilla, P AU - Brambilla P AD - Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy; Scientific Institute IRCCS "E. Medea", Bosisio Parini (Lc), Italy. Electronic address: paolo.brambilla1@unimi.it. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review DEP - 20180724 PL - Netherlands TA - J Affect Disord JT - Journal of affective disorders JID - 7906073 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 7171WSG8A2 (BDNF protein, human) SB - IM MH - Adolescent MH - Adult MH - Alleles MH - Anxiety Disorders/genetics MH - Bipolar Disorder/*genetics/metabolism MH - Brain-Derived Neurotrophic Factor/*genetics MH - Child MH - Executive Function MH - Female MH - Humans MH - Male MH - Middle Aged MH - Mood Disorders/*genetics/metabolism MH - *Polymorphism, Genetic MH - Polymorphism, Single Nucleotide OTO - NOTNLM OT - BDNF OT - Bipolar Disorder OT - Cognition OT - Single-nucleotide polymorphism EDAT- 2018/08/07 06:00 MHDA- 2019/02/28 06:00 CRDT- 2018/08/07 06:00 PHST- 2018/04/27 00:00 [received] PHST- 2018/07/12 00:00 [revised] PHST- 2018/07/20 00:00 [accepted] PHST- 2018/08/07 06:00 [pubmed] PHST- 2019/02/28 06:00 [medline] PHST- 2018/08/07 06:00 [entrez] AID - S0165-0327(18)30909-1 [pii] AID - 10.1016/j.jad.2018.07.054 [doi] PST - ppublish SO - J Affect Disord. 2019 Jan 15;243:552-558. doi: 10.1016/j.jad.2018.07.054. Epub 2018 Jul 24.