English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Association between hippocampal structure and serum Brain-Derived Neurotrophic Factor (BDNF) in healthy adults: A registered report

MPS-Authors
/persons/resource/persons181261

Puhlmann,  Lara M.
Research Group Social Stress and Family Health, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Leibniz Institute for Resilience Research (LIR), Mainz, Germany;

/persons/resource/persons185220

Linz,  Roman
Research Group Social Stress and Family Health, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

/persons/resource/persons71665

Valk,  Sofie L.
Institute of Systems Neuroscience, University Hospital Düsseldorf, Germany;
Institute of Neuroscience and Medicine, Research Center Jülich, Germany;
Otto Hahn Group Cognitive Neurogenetics, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

/persons/resource/persons129987

Vrticka,  Pascal
Research Group Social Stress and Family Health, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Department of Psychology, University of Essex, Colchester, United Kingdom;

/persons/resource/persons20000

Singer,  Tania
Social Neuroscience Lab, Max Planck Society;

/persons/resource/persons19628

Engert,  Veronika
Research Group Social Stress and Family Health, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Institute of Psychosocial Medicine and Psychotherapy, Jena University Hospital, Germany;

External Resource
No external resources are shared
Fulltext (public)

Puhlmann_2021.pdf
(Publisher version), 3MB

Supplementary Material (public)
There is no public supplementary material available
Citation

Puhlmann, L. M., Linz, R., Valk, S. L., Vrticka, P., Vos de Wael, R., Bernasconi, A., et al. (2021). Association between hippocampal structure and serum Brain-Derived Neurotrophic Factor (BDNF) in healthy adults: A registered report. NeuroImage, 236: 118011. doi:10.1016/j.neuroimage.2021.118011.


Cite as: http://hdl.handle.net/21.11116/0000-0004-D535-0
Abstract
The hippocampus is a highly plastic brain structure supporting functions central to human cognition. Morphological changes in the hippocampus have been implicated in development, aging, as well as in a broad range of neurological and psychiatric disorders. A growing body of research suggests that hippocampal plasticity is closely linked to the actions of brain-derived neurotrophic factor (BDNF). However, evidence on the relationship between hippocampal volume (HCV) and peripheral BDNF levels is scarce and limited to elderly and patient populations. Further, despite evidence that BDNF expression differs throughout the hippocampus and is implicated in adult neurogenesis specifically in the dentate gyrus, no study has so far related peripheral BDNF levels to the volumes of individual hippocampal subfields. Besides its clinical implications, BDNF-facilitated hippocampal plasticity plays an important role in regulating cognitive and affective processes. In the current registered report, we investigated how serum BDNF (sBDNF) levels relate to volumes of the hippocampal formation and its subfields in a large sample of healthy adults (N = 279, 160 f) with a broad age range (20–55 years, mean 40.5) recruited in the context of the ReSource Project. We related HCV to basal sBDNF and, in a subsample (n = 103, 57 f), to acute stress-reactive change in sBDNF. We further tested the role of age as a moderator of both associations. Contrary to our hypotheses, neither basal sBDNF levels nor stress-reactive sBDNF change were associated with total HCV or volume of the dentate gyrus/cornu ammonis 4 (DG/CA4) subfield. We also found no evidence for a moderating effect of age on any of these associations. Our null results provide a first point of reference on the relationship between sBDNF and HCV in healthy mid-age, in contrast to patient or aging populations. We suggest that sBDNF levels have limited predictive value for morphological differences of the hippocampal structure when notable challenge to its neuronal integrity or to neurotrophic capacity is absent.