BDNF Val66Met, Aβ amyloid, and cognitive decline in preclinical Alzheimer's disease

Yen Ying Lim*, Victor L. Villemagne, Simon M. Laws, David Ames, Robert H. Pietrzak, Kathryn A. Ellis, Karra D. Harrington, Pierrick Bourgeat, Olivier Salvado, David Darby, Peter J. Snyder, Ashley I. Bush, Ralph N. Martins, Colin L. Masters, Christopher C. Rowe, Pradeep J. Nathan, Paul Maruff

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

96 Citations (Scopus)


Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism has previously been implicated in Alzheimer's disease (AD)-related cognitive impairment. We aimed to determine the relationship between BDNF Val66Met and beta-amyloid (Aβ) on cognitive decline, hippocampal atrophy, and Aβ accumulation over 36 months in 165 healthy adults enrolled in the Australian Imaging, Biomarkers and Lifestyle study. In healthy adults with high Aβ, Met carriers showed significant and moderate-to-large declines in episodic memory, executive function, and language, and greater hippocampal atrophy over 36 months, compared with Val/Val homozygotes. BDNF Val66Met was not found to be related to rates of change in cognition or hippocampal volume in healthy adults with low Aβ. BDNF Val66Met did not relate to the amount of Aβ or to the rate of Aβ accumulation in either group. High Aβ levels coupled with Met carriage may be useful prognostic markers of accelerated cognitive decline and hippocampal degeneration in individuals in the preclinical stage of AD.

Original languageEnglish
Pages (from-to)2457-2464
Number of pages8
JournalNeurobiology of Aging
Issue number11
Publication statusPublished - Nov 2013
Externally publishedYes


  • Aβ accumulation
  • BDNF Val66Met
  • Beta-Amyloid
  • Cognitive decline
  • Healthy older adults
  • Hippocampal atrophy
  • Preclinical Alzheimer's disease


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