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Lack of neural compensatory mechanisms of BDNF val66met met carriers and APOE E4 carriers in healthy aging, mild cognitive impairment, and Alzheimer's disease.
Neurobiol Aging. 2016 Mar; 39:165-73.NA

Abstract

Compromises in compensatory neurobiologic mechanisms due to aging and/or genetic factors (i.e., APOE gene) may influence brain-derived neurotrophic factor (BDNF) val66met polymorphism effects on temporal lobe morphometry and memory performance. We studied 2 cohorts from Alzheimer's Disease Neuroimaging Initiative: 175 healthy subjects and 222 with prodromal and established Alzheimer's disease. Yearly structural magnetic resonance imaging and cognitive performance assessments were carried out over 3 years of follow-up. Both cohorts had similar BDNF Val/Val and Met allele carriers' (including both Val/Met and Met/Met individuals) distribution. In healthy subjects, a significant trend for thinner posterior cingulate and precuneus cortices was detected in Met carriers compared to Val homozygotes in APOE E4 carriers, with large and medium effect sizes, respectively. The mild cognitive impairment/Alzheimer's disease cohort showed a longitudinal decline in entorhinal thickness in BDNF Met carriers compared to Val/Val in APOE E4 carriers, with effect sizes ranging from medium to large. In addition, an effect of BDNF genotype was found in APOE E4 carriers for episodic memory (logical memory and ADAS-Cog) and semantic fluency measures, with Met carriers performing worse in all cases. These findings suggest a lack of compensatory mechanisms in BDNF Met carriers and APOE E4 carriers in healthy and pathological aging.

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Authors+Show Affiliations

Gomar JJ
The Litwin-Zucker Alzheimer's Disease Research Center, The Feinstein Institute for Medical Research, Manhasset, NY, USA; FIDMAG Hermanas Hospitalarias Research Foundation & CIBERSAM, Sant Boi de Llobregat, Spain.
Conejero-Goldberg C
The Litwin-Zucker Alzheimer's Disease Research Center, The Feinstein Institute for Medical Research, Manhasset, NY, USA.
Huey ED
Taub Institute for Research on Alzheimer's disease and the Aging Brain, The Gertrude H. Sergievsky Center, Columbia University, New York, NY, USA; College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Davies P
The Litwin-Zucker Alzheimer's Disease Research Center, The Feinstein Institute for Medical Research, Manhasset, NY, USA; Hofstra North Shore LIJ School of Medicine, Hempstead, NY, USA.
Goldberg TE
The Litwin-Zucker Alzheimer's Disease Research Center, The Feinstein Institute for Medical Research, Manhasset, NY, USA; Hofstra North Shore LIJ School of Medicine, Hempstead, NY, USA. Electronic address: tgoldber@nshs.edu.
Alzheimer's Disease Neuroimaging Initiative
No affiliation info available

MeSH

AgedAged, 80 and overAgingAlzheimer DiseaseApolipoproteins EBrainBrain-Derived Neurotrophic FactorCognitionCognitive DysfunctionCohort StudiesFemaleGenotypeHeterozygoteHumansMagnetic Resonance ImagingMaleMemory, EpisodicMiddle AgedNeuroimagingPolymorphism, Genetic

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26923413

Citation

Gomar, Jesus J., et al. "Lack of Neural Compensatory Mechanisms of BDNF Val66met Met Carriers and APOE E4 Carriers in Healthy Aging, Mild Cognitive Impairment, and Alzheimer's Disease." Neurobiology of Aging, vol. 39, 2016, pp. 165-73.
Gomar JJ, Conejero-Goldberg C, Huey ED, et al. Lack of neural compensatory mechanisms of BDNF val66met met carriers and APOE E4 carriers in healthy aging, mild cognitive impairment, and Alzheimer's disease. Neurobiol Aging. 2016;39:165-73.
Gomar, J. J., Conejero-Goldberg, C., Huey, E. D., Davies, P., & Goldberg, T. E. (2016). Lack of neural compensatory mechanisms of BDNF val66met met carriers and APOE E4 carriers in healthy aging, mild cognitive impairment, and Alzheimer's disease. Neurobiology of Aging, 39, 165-73. https://doi.org/10.1016/j.neurobiolaging.2015.12.004
Gomar JJ, et al. Lack of Neural Compensatory Mechanisms of BDNF Val66met Met Carriers and APOE E4 Carriers in Healthy Aging, Mild Cognitive Impairment, and Alzheimer's Disease. Neurobiol Aging. 2016;39:165-73. PubMed PMID: 26923413.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lack of neural compensatory mechanisms of BDNF val66met met carriers and APOE E4 carriers in healthy aging, mild cognitive impairment, and Alzheimer's disease. AU - Gomar,Jesus J, AU - Conejero-Goldberg,Concepcion, AU - Huey,Edward D, AU - Davies,Peter, AU - Goldberg,Terry E, AU - ,, Y1 - 2015/12/19/ PY - 2015/06/17/received PY - 2015/11/02/revised PY - 2015/12/14/accepted PY - 2016/3/1/entrez PY - 2016/3/1/pubmed PY - 2016/12/15/medline KW - AD KW - APOE KW - Aging KW - BDNF KW - Brain morphometry KW - Cognition KW - MCI SP - 165 EP - 73 JF - Neurobiology of aging JO - Neurobiol Aging VL - 39 N2 - Compromises in compensatory neurobiologic mechanisms due to aging and/or genetic factors (i.e., APOE gene) may influence brain-derived neurotrophic factor (BDNF) val66met polymorphism effects on temporal lobe morphometry and memory performance. We studied 2 cohorts from Alzheimer's Disease Neuroimaging Initiative: 175 healthy subjects and 222 with prodromal and established Alzheimer's disease. Yearly structural magnetic resonance imaging and cognitive performance assessments were carried out over 3 years of follow-up. Both cohorts had similar BDNF Val/Val and Met allele carriers' (including both Val/Met and Met/Met individuals) distribution. In healthy subjects, a significant trend for thinner posterior cingulate and precuneus cortices was detected in Met carriers compared to Val homozygotes in APOE E4 carriers, with large and medium effect sizes, respectively. The mild cognitive impairment/Alzheimer's disease cohort showed a longitudinal decline in entorhinal thickness in BDNF Met carriers compared to Val/Val in APOE E4 carriers, with effect sizes ranging from medium to large. In addition, an effect of BDNF genotype was found in APOE E4 carriers for episodic memory (logical memory and ADAS-Cog) and semantic fluency measures, with Met carriers performing worse in all cases. These findings suggest a lack of compensatory mechanisms in BDNF Met carriers and APOE E4 carriers in healthy and pathological aging. SN - 1558-1497 UR - https://www.unboundmedicine.com/medline/citation/26923413/Lack_of_neural_compensatory_mechanisms_of_BDNF_val66met_met_carriers_and_APOE_E4_carriers_in_healthy_aging_mild_cognitive_impairment_and_Alzheimer's_disease_ DB - PRIME DP - Unbound Medicine ER -