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Decreased medial temporal lobe activation in BDNF 66Met allele carriers during memory encoding
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Physiology. Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI).
Stockholm University.
Umeå University, Faculty of Medicine, Department of Clinical Sciences, Psychiatry.
Umeå University, Faculty of Social Sciences, Umeå School of Business and Economics (USBE), Statistics. Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Physiology. Umeå University, Faculty of Medicine, Umeå Centre for Functional Brain Imaging (UFBI).ORCID iD: 0000-0003-1524-0851
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2013 (English)In: Neuropsychologia, ISSN 0028-3932, E-ISSN 1873-3514, Vol. 51, no 12, 2462-2468 p.Article in journal (Refereed) Published
Abstract [en]

The Met allele of the Brain-derived neurotrophic factor (BDNF) Val(66)Met polymorphism has been associated with impaired activity-dependent secretion of BDNF protein and decreased memory performance. Results from imaging studies relating Val(66)Met to brain activation during memory processing have been inconsistent, with reports of both increased and decreased activation in the Medial Temporal Lobe (MTL) in Met carriers relative to Val homozygotes. Here, we extensively studied BDNF Val(66)Met in relation to brain activation and white matter integrity as well as memory performance in a large imaging (n=194) and behavioral (n=2229) sample, respectively. Functional magnetic resonance imaging (fMRI) was used to investigate MTL activation in healthy participants in the age of 55-75 years during a face-name episodic encoding and retrieval task. White matter integrity was measured using diffusion tensor imaging.

BDNF Met allele carriers had significantly decreased activation in the MTL during encoding processes, but not during retrieval processes. In contrast to previous proposals, the effect was not modulated by age and the polymorphism was not related to white matter integrity. Met carriers had lower memory performance than Val homozygotes, but differences were subtle and not significant. In conclusion, the BDNF Met allele has a negative influence on MTL functioning, preferentially during encoding processes, which might translate into impaired episodic memory function.

Place, publisher, year, edition, pages
Elsevier, 2013. Vol. 51, no 12, 2462-2468 p.
Keyword [en]
imaging, genetics, memory, Val66Met, Parahippocampus
National Category
Neurosciences
Research subject
Physiology
Identifiers
URN: urn:nbn:se:umu:diva-71132DOI: 10.1016/j.neuropsychologia.2012.11.028ISI: 000328526800014OAI: oai:DiVA.org:umu-71132DiVA: diva2:622057
Available from: 2013-05-20 Created: 2013-05-20 Last updated: 2017-12-06Bibliographically approved
In thesis
1. Genes to remember: imaging genetics of hippocampus-based memory functions
Open this publication in new window or tab >>Genes to remember: imaging genetics of hippocampus-based memory functions
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

In the field of imaging genetics, brain function and structure are used as intermediate phenotypes between genes and cognition/diseases to validate and extend findings from behavioral genetics. In this thesis, three of the strongest candidate genes for episodic memory, KIBRA, BDNF, and APOE, were examined in relation to memory performance and hippocampal/parahippocampal fMRI blood-oxygen level-dependent (BOLD) signal. A common T allele in the KIBRA gene was previously associated with superior memory, and increased hippocampal activation was observed in noncarriers of the T allele which was interpreted as reflecting compensatory recruitment. The results from the first study revealed that both memory performance and hippocampal activation at retrieval was higher in T allele carriers (study I). The BDNF 66Met and APOE ε4 alleles have previously been associated with poorer memory performance, but their relation to brain activation has been inconsistent with reports of both increased and decreased regional brain activation relative to noncarriers. Here, decreased hippocampal/parahippocampal activation was observed in carriers of BDNF 66Met (study II) as well as APOE ε4 (study III) during memory encoding. In addition, there was an additive gene-gene effect of APOE and BDNF on hippocampal and parahippocampal activation (study III). Collectively, the results from these studies on KIBRA, BDNF, and APOE converge on higher medial temporal lobe activation for carriers of a high-memory associated allele, relative to carriers of a low-memory associated allele. In addition, the observed additive effect of APOE and BDNF demonstrate that a larger amount of variance in BOLD signal change can be explained by considering the combined effect of more than one genetic polymorphism. These imaging genetics findings support and extend previous knowledge from behavioral genetics on the role of these memory-related genes.

Place, publisher, year, edition, pages
Umeå: Umeå Universitet, 2013. 84 p.
Series
Umeå University medical dissertations, ISSN 0346-6612 ; 1580
Keyword
Imaging genetics, fMRI, Episodic memory, SNP, KIBRA, BDNF, APOE, Hippocampus, Parahippocampus
National Category
Neurosciences
Identifiers
urn:nbn:se:umu:diva-71141 (URN)978-91-7459-598-7 (ISBN)978-91-7459-597-0 (ISBN)
Public defence
2013-06-14, BiA 201, Biologihuset, Umeå universitet, Umeå, 10:00 (English)
Opponent
Supervisors
Available from: 2013-05-24 Created: 2013-05-20 Last updated: 2015-04-30Bibliographically approved

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Publisher's full texthttp://www.sciencedirect.com/science/article/pii/S0028393212005052

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Kauppi, KarolinaAdolfsson, RolfLundquist, AndersNyberg, Lars

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