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Performance-related increases in hippocampal N-acetylaspartate (NAA) induced by spatial navigation training are restricted to BDNF Val Homozygotes

Martin Lövden, Sabine Schäfer, Hannes Noack, Nils Bodammer, Simone Kühn UGent, Martin Kanowski, Jörn Kaufmann, Claus Tempelmann, H-J Heinze and Emrah Düzel, et al. (2011) CEREBRAL CORTEX. 21(6). p.1435-1442
abstract
Recent evidence indicates experience-dependent brain volume changes in humans, but the functional and histological nature of such changes is unknown. Here, we report that adult men performing a cognitively demanding spatial navigation task every other day over 4 months display increases in hippocampal N-acetylaspartate (NAA) as measured with magnetic resonance spectroscopy. Unlike measures of brain volume, changes in NAA are sensitive to metabolic and functional aspects of neural and glia tissue and unlikely to reflect changes in microvasculature. Training-induced changes in NAA were, however, absent in carriers of the Met substitution in the brain-derived neurotrophic factor (BDNF) gene, which is known to reduce activity-dependent secretion of BDNF. Among BDNF Val homozygotes, increases in NAA were strongly related to the degree of practice-related improvement in navigation performance and normalized to pretraining levels 4 months after the last training session. We conclude that changes in demands on spatial navigation can alter hippocampal NAA concentrations, confirming epidemiological studies suggesting that mental experience may have direct effects on neural integrity and cognitive performance. BDNF genotype moderates these plastic changes, in line with the contention that gene-context interactions shape the ontogeny of complex phenotypes.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
VAL66MET POLYMORPHISM, ACTIVITY-DEPENDENT SECRETION, NEUROTROPHIC FACTOR, TAXI DRIVERS, HUMAN-MEMORY, BRAIN, PLASTICITY, EXPERIENCE, STRATEGIES, NEURONS, brain-derived neurotrophic factor (BDNF), cognitive training, hippocampus, N-acetylaspartate (NAA), spatial navigation
journal title
CEREBRAL CORTEX
Cereb. Cortex
volume
21
issue
6
pages
1435 - 1442
Web of Science type
Article
Web of Science id
000290853300018
JCR category
NEUROSCIENCES
JCR impact factor
6.544 (2011)
JCR rank
22/242 (2011)
JCR quartile
1 (2011)
ISSN
1047-3211
DOI
10.1093/cercor/bhq230
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1090306
handle
http://hdl.handle.net/1854/LU-1090306
date created
2010-12-21 09:20:21
date last changed
2012-07-01 00:30:28
@article{1090306,
  abstract     = {Recent evidence indicates experience-dependent brain volume changes in humans, but the functional and histological nature of such changes is unknown. Here, we report that adult men performing a cognitively demanding spatial navigation task every other day over 4 months display increases in hippocampal N-acetylaspartate (NAA) as measured with magnetic resonance spectroscopy. Unlike measures of brain volume, changes in NAA are sensitive to metabolic and functional aspects of neural and glia tissue and unlikely to reflect changes in microvasculature. Training-induced changes in NAA were, however, absent in carriers of the Met substitution in the brain-derived neurotrophic factor (BDNF) gene, which is known to reduce activity-dependent secretion of BDNF. Among BDNF Val homozygotes, increases in NAA were strongly related to the degree of practice-related improvement in navigation performance and normalized to pretraining levels 4 months after the last training session. We conclude that changes in demands on spatial navigation can alter hippocampal NAA concentrations, confirming epidemiological studies suggesting that mental experience may have direct effects on neural integrity and cognitive performance. BDNF genotype moderates these plastic changes, in line with the contention that gene-context interactions shape the ontogeny of complex phenotypes.},
  author       = {L{\"o}vden, Martin and Sch{\"a}fer, Sabine and Noack, Hannes  and Bodammer, Nils and K{\"u}hn, Simone and Kanowski, Martin and Kaufmann, J{\"o}rn and Tempelmann, Claus and Heinze, H-J and D{\"u}zel, Emrah and B{\"a}ckmann, Lars and Lindenberger, Ulman},
  issn         = {1047-3211},
  journal      = {CEREBRAL CORTEX},
  keyword      = {VAL66MET POLYMORPHISM,ACTIVITY-DEPENDENT SECRETION,NEUROTROPHIC FACTOR,TAXI DRIVERS,HUMAN-MEMORY,BRAIN,PLASTICITY,EXPERIENCE,STRATEGIES,NEURONS,brain-derived neurotrophic factor (BDNF),cognitive training,hippocampus,N-acetylaspartate (NAA),spatial navigation},
  language     = {eng},
  number       = {6},
  pages        = {1435--1442},
  title        = {Performance-related increases in hippocampal N-acetylaspartate (NAA) induced by spatial navigation training are restricted to BDNF Val Homozygotes},
  url          = {http://dx.doi.org/10.1093/cercor/bhq230},
  volume       = {21},
  year         = {2011},
}

Chicago
Lövden, Martin, Sabine Schäfer, Hannes Noack, Nils Bodammer, Simone Kühn, Martin Kanowski, Jörn Kaufmann, et al. 2011. “Performance-related Increases in Hippocampal N-acetylaspartate (NAA) Induced by Spatial Navigation Training Are Restricted to BDNF Val Homozygotes.” Cerebral Cortex 21 (6): 1435–1442.
APA
Lövden, M., Schäfer, S., Noack, H., Bodammer, N., Kühn, S., Kanowski, M., Kaufmann, J., et al. (2011). Performance-related increases in hippocampal N-acetylaspartate (NAA) induced by spatial navigation training are restricted to BDNF Val Homozygotes. CEREBRAL CORTEX, 21(6), 1435–1442.
Vancouver
1.
Lövden M, Schäfer S, Noack H, Bodammer N, Kühn S, Kanowski M, et al. Performance-related increases in hippocampal N-acetylaspartate (NAA) induced by spatial navigation training are restricted to BDNF Val Homozygotes. CEREBRAL CORTEX. 2011;21(6):1435–42.
MLA
Lövden, Martin, Sabine Schäfer, Hannes Noack, et al. “Performance-related Increases in Hippocampal N-acetylaspartate (NAA) Induced by Spatial Navigation Training Are Restricted to BDNF Val Homozygotes.” CEREBRAL CORTEX 21.6 (2011): 1435–1442. Print.