BDNF Val66Met moderates memory impairment, hippocampal function and tau in preclinical autosomal dominant Alzheimer’s disease
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See Rogaeva and Schmitt-Ulms (doi: 10.1093/aww201 ) for a scientific commentary on this article . The brain-derived neurotrophic factor ( BDNF ) Val66Met polymorphism is implicated in synaptic excitation and neuronal integrity, and has previously been shown to moderate amyloid-β-related memory decline and hippocampal atrophy in preclinical sporadic Alzheimer’s disease. However, the effect of BDNF in autosomal dominant Alzheimer’s disease is unknown. We aimed to determine the effect of BDNF Val66Met on cognitive function, hippocampal function, tau and amyloid-β in preclinical autosomal dominant Alzheimer’s disease. We explored effects of apolipoprotein E ( APOE ) ε4 on these relationships. The Dominantly Inherited Alzheimer Network conducted clinical, neuropsychological, genetic, biomarker and neuroimaging measures at baseline in 131 mutation non-carriers and 143 preclinical autosomal dominant Alzheimer’s disease mutation carriers on average 12 years before clinical symptom onset. BDNF genotype data were obtained for mutation carriers (95 Val 66 homozygotes, 48 Met 66 carriers). Among preclinical mutation carriers, Met 66 carriers had worse memory performance, lower hippocampal glucose metabolism and increased levels of cerebrospinal fluid tau and phosphorylated tau (p-tau) than Val 66 homozygotes. Cortical amyloid-β and cerebrospinal fluid amyloid-β 42 levels were significantly different from non-carriers but did not differ between preclinical mutation carrier Val 66 homozygotes and Met 66 carriers. There was an effect of APOE on amyloid-β levels, but not cognitive function, glucose metabolism or tau. As in sporadic Alzheimer’s disease, the deleterious effects of amyloid-β on memory, hippocampal function, and tau in preclinical autosomal dominant Alzheimer’s disease mutation carriers are greater in Met 66 carriers. To date, this is the only genetic factor found to moderate downstream effects of amyloid-β in autosomal dominant Alzheimer’s disease. See Rogaeva and Schmitt-Ulms (doi: 10.1093/aww201 ) for a scientific commentary on this article . The brain-derived neurotrophic factor (BDNF) Val66Met polymorphism modulates Aβ+ related memory decline in sporadic Alzheimer’s disease. Yen Ying Lim et al. report that this polymorphism also affects outcomes in autosomal dominant Alzheimer’s disease. Met66 carriers show greater dysfunction in cognition, glucose metabolism and tau, with implications for clinical trial design.
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The cognitive composite used here is a reliable detector of decline across the EYO and CDR range.
“we developed a cognitive composite that reliably detects decline across the range of EYO and CDR values57.”
From A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease (2020) · cites this paper as [57]
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Self-citationBDNF VAL66MET polymorphism and memory decline across the spectrum of Alzheimer's disease
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15 years of longitudinal genetic, clinical, cognitive, imaging, and biochemical measures in DIAN
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DAT1 and BDNF polymorphisms interact to predict Aβ and tau pathology
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Self-citationDoesBDNFVal66Met contribute to preclinical Alzheimer’s disease?
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Neuroimaging within the Dominantly Inherited Alzheimer’s Network (DIAN): PET and MRIPreprint
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Distinct Patterns Link the BDNF Val66Met Polymorphism to Alzheimer’s Disease Pathology
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BDNF–amyloid-β Axis in Alzheimer’s disease: molecular mechanisms and therapeutic perspectives
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- Authors
- Lim, Y. Y., Hassenstab, J., Cruchaga, C., Goate, A., Fagan, A. M., Benzinger, T. L. S., Maruff, P., Snyder, P. J., Masters, C. L., Allegri, R., Chhatwal, J., Farlow, M. R., Graff-Radford, N. R., Laske, C., Levin, J., McDade, E., Ringman, J. M., Rossor, M., Salloway, S., Schofield, P. R., Holtzman, D. M., Morris, J. C., & Bateman, R. J.
- Affiliations
- The University of Melbourne (AU)
- Washington University in St. Louis (US)
- Icahn School of Medicine at Mount Sinai (US)
- Brown University (US)
- Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia (AR)
- Brigham and Women's Hospital (US)
- Indiana University Indianapolis (US)
- German Center for Neurodegenerative Diseases (DE)
- Ludwig-Maximilians-Universität München (DE)
- University of Southern California (US)
- UCL Queen Square Institute of Neurology (GB)
- UNSW Sydney (AU)
- ORCID
- Lim, Yen Ying
- Hassenstab, Jason
- Cruchaga, Carlos
- Goate, Alison
- Fagan, Anne M.
- Benzinger, Tammie L. S.
- Maruff, Paul
- Snyder, Peter J.
- Masters, Colin L.
- Allegri, Ricardo
- Chhatwal, Jasmeer
- Farlow, Martin R.
- Laske, Christoph
- Levin, Johannes
- McDade, Eric
- Ringman, John M.
- Rossor, Martin
- Salloway, Stephen
- Schofield, Peter R.
- Holtzman, David M.
- Morris, John C.
- Bateman, Randall J.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-08-12
- Volume
- 139
- Issue
- 10
- Pages
- 2766-2777
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC5815565
- OpenAlex
- W2510233326
- Cited by
- 76
- References
- 49
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 2 · 2023: 5 · 2022: 14 · 2021: 10 · 2020: 13 · 2019: 7 · 2018: 12 · 2017: 4 · 2016: 2
- FWCI
- 6.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- DZNE Pub (submittedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Purdue University Indianapolis (Indiana University) (submittedVersion)
- Funders
- National Institute for Health and Care Research (NF-SI-0512-10033)
- National Institutes of Health (UL1TR000448)
- Medical Research Council (MR/L023784/2, MR/L023784/1)
- National Institute on Aging (UF1AG032438, P50AG005142, U19AG032438, U24AG021886)
- National Cancer Institute (P30CA091842)
- National Institute of Diabetes and Digestive and Kidney Diseases (K23DK094982)
- National Institute of Biomedical Imaging and Bioengineering (R01EB009352)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- BDNF Val66Met polymorphism, autosomal dominant Alzheimer's disease, preclinical Alzheimer's disease, memory impairment, tau protein, phosphorylated tau, amyloid-beta, APOE ε4, genetic moderation, cerebrospinal fluid biomarkers, amyloid-beta 42
- MeSH terms
- Adult, Alzheimer Disease, Female, Heterozygote, Hippocampus, Humans, Male, Memory Disorders, Methionine, Middle Aged, Valine, tau Proteins, Brain-Derived Neurotrophic Factor
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