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Title: BDNF Val66Met in preclinical Alzheimer's disease is associated with short-term changes in episodic memory and hippocampal volume but not serum mBDNF.
Austin Authors: Lim, Yen Ying;Rainey-Smith, Stephanie R;Lim, Yoon;Laws, Simon M;Gupta, Veer;Porter, Tenielle;Bourgeat, Pierrick;Ames, David;Fowler, Christopher;Salvado, Olivier;Villemagne, Victor L ;Rowe, Christopher C ;Masters, Colin L ;Zhou, Xin Fu;Martins, Ralph N;Maruff, Paul
Affiliation: Centre of Excellence for Alzheimer's Disease Research and Care, Edith Cowan University, Joondalup, Western Australia, Australia
School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia
Commonwealth Scientific Industrial Research Organization (CSIRO) Preventative Health National Research Flagship, Australian e-Health Research Centre-BiaMedIA, Brisbane, Queensland, Australia
Academic Unit for Psychiatry of Old Age, St. Vincent's Health, The University of Melbourne, Kew, Victoria, Australia
Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia
The Florey Institute, The University of Melbourne, Parkville, Victoria, Australia
Issue Date: Nov-2017 2017-07-19
Publication information: International psychogeriatrics 2017; 29(11): 1825-1834
Abstract: The brain-derived neurotrophic factor (BDNF) Val66Met polymorphism Met allele exacerbates amyloid (Aβ) related decline in episodic memory (EM) and hippocampal volume (HV) over 36-54 months in preclinical Alzheimer's disease (AD). However, the extent to which Aβ+ and BDNF Val66Met is related to circulating markers of BDNF (e.g. serum) is unknown. We aimed to determine the effect of Aβ and the BDNF Val66Met polymorphism on levels of serum mBDNF, EM, and HV at baseline and over 18-months. Non-demented older adults (n = 446) underwent Aβ neuroimaging and BDNF Val66Met genotyping. EM and HV were assessed at baseline and 18 months later. Fasted blood samples were obtained from each participant at baseline and at 18-month follow-up. Aβ PET neuroimaging was used to classify participants as Aβ- or Aβ+. At baseline, Aβ+ adults showed worse EM impairment and lower serum mBDNF levels relative to Aβ- adults. BDNF Val66Met polymorphism did not affect serum mBDNF, EM, or HV at baseline. When considered over 18-months, compared to Aβ- Val homozygotes, Aβ+ Val homozygotes showed significant decline in EM and HV but not serum mBDNF. Similarly, compared to Aβ+ Val homozygotes, Aβ+ Met carriers showed significant decline in EM and HV over 18-months but showed no change in serum mBDNF. While allelic variation in BDNF Val66Met may influence Aβ+ related neurodegeneration and memory loss over the short term, this is not related to serum mBDNF. Longer follow-up intervals may be required to further determine any relationships between serum mBDNF, EM, and HV in preclinical AD.
DOI: 10.1017/S1041610217001284
ORCID: 0000-0003-3910-2453
Journal: International psychogeriatrics
PubMed URL: 28720165
Type: Journal Article
Subjects: Alzheimer's disease
brain-derived neurotrophic factor
hippocampal volume
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