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The BDNFVal66Met SNP modulates the association between beta-amyloid and hippocampal disconnection in Alzheimer's disease. 2021
Nicolai Franzmeier, and
Jinyi Ren, and
Alexander Damm, and
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Alfredo Ramirez, and
Frank Jessen, and
Emrah Düzel, and
Octavio Rodríguez Gómez, and
Tammie Benzinger, and
Alison Goate, and
Celeste M Karch, and
Anne M Fagan, and
Eric McDade, and
Katharina Buerger, and
Johannes Levin, and
Marco Duering, and
Martin Dichgans, and
Marc Suárez-Calvet, and
Christian Haass, and
Brian A Gordon, and
Yen Ying Lim, and
Colin L Masters, and
Daniel Janowitz, and
Cihan Catak, and
Steffen Wolfsgruber, and
Michael Wagner, and
Esther Milz, and
Sonia Moreno-Grau, and
Stefan Teipel, and
Michel J Grothe, and
Ingo Kilimann, and
Martin Rossor, and
Nick Fox, and
Christoph Laske, and
Jasmeer Chhatwal, and
Peter Falkai, and
Robert Perneczky, and
Jae-Hong Lee, and
Annika Spottke, and
Henning Boecker, and
Frederic Brosseron, and
Klaus Fliessbach, and
Michael T Heneka, and
Peter Nestor, and
Oliver Peters, and
Manuel Fuentes, and
Felix Menne, and
Josef Priller, and
Eike J Spruth, and
Christiana Franke, and
Anja Schneider, and
Christine Westerteicher, and
Oliver Speck, and
Jens Wiltfang, and
Claudia Bartels, and
Miguel Ángel Araque Caballero, and
Coraline Metzger, and
Daniel Bittner, and
Stephen Salloway, and
Adrian Danek, and
Jason Hassenstab, and
Igor Yakushev, and
Peter R Schofield, and
John C Morris, and
Randall J Bateman, and
Michael Ewers
Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-Universität LMU, Munich, Germany.
In Alzheimer's disease (AD), a single-nucleotide polymorphism in the gene encoding brain-derived neurotrophic factor (BDNFVal66Met) is associated with worse impact of primary AD pathology (beta-amyloid, Aβ) on neurodegeneration and cognitive decline, rendering BDNFVal66Met an important modulating factor of cognitive impairment in AD. However, the effect of BDNFVal66Met on functional networks that may underlie cognitive impairment in AD is poorly understood. Using a cross-validation approach, we first explored in subjects with autosomal dominant AD (ADAD) from the Dominantly Inherited Alzheimer Network (DIAN) the effect of BDNFVal66Met on resting-state fMRI assessed functional networks. In seed-based connectivity analysis of six major large-scale networks, we found a stronger decrease of hippocampus (seed) to medial-frontal connectivity in the BDNFVal66Met carriers compared to BDNFVal homozogytes. BDNFVal66Met was not associated with connectivity in any other networks. Next, we tested whether the finding of more pronounced decrease in hippocampal-medial-frontal connectivity in BDNFVal66Met could be also found in elderly subjects with sporadically occurring Aβ, including a group with subjective cognitive decline (N = 149, FACEHBI study) and a group ranging from preclinical to AD dementia (N = 114, DELCODE study). In both of these independently recruited groups, BDNFVal66Met was associated with a stronger effect of more abnormal Aβ-levels (assessed by biofluid-assay or amyloid-PET) on hippocampal-medial-frontal connectivity decreases, controlled for hippocampus volume and other confounds. Lower hippocampal-medial-frontal connectivity was associated with lower global cognitive performance in the DIAN and DELCODE studies. Together these results suggest that BDNFVal66Met is selectively associated with a higher vulnerability of hippocampus-frontal connectivity to primary AD pathology, resulting in greater AD-related cognitive impairment.
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