Literature DB >> 28764930

Association between educational attainment and amyloid deposition across the spectrum from normal cognition to dementia: neuroimaging evidence for protection and compensation.

Eider M Arenaza-Urquijo1, Alexandre Bejanin2, Julie Gonneaud2, Miranka Wirth2, Renaud La Joie2, Justine Mutlu2, Malo Gaubert2, Brigitte Landeau2, Vincent de la Sayette3, Francis Eustache2, Gaël Chételat2.   

Abstract

The brain mechanisms underlying the effect of intellectual enrichment may evolve along the normal aging Alzheimer's disease (AD) cognitive spectrum and may include both protective and compensatory mechanisms. We assessed the association between early intellectual enrichment (education, years) and average cortical florbetapir standardized uptake value ratio as well as performed voxel-wise analyses in a total of 140 participants, including cognitively normal older adults, mild cognitive impairment (MCI), and AD patients. Higher education was associated with lower cortical florbetapir positron emission tomography (florbetapir-PET) uptake, notably in the frontal lobe in normal older adults, but with higher uptake in frontal, temporal, and parietal regions in MCI after controlling for global cognitive status. No association was found in AD. In MCI, we observed an increased fluorodeoxyglucose positron emission tomography (FDG-PET) uptake with education within the regions of higher florbetapir-PET uptake, suggesting a compensatory increase. Early intellectual enrichment may be associated with protection and compensation for amyloid beta (Aβ) deposition later in life, before the onset of dementia. Previous investigations have been controversial as regard to the effects of intellectual enrichment variables on Aβ deposition; the present findings call for approaches aiming to evaluate mechanisms of resilience across disease stages.
Copyright © 2017 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Alzheimer's disease; Amyloid; Cognitive reserve; Compensation; Glucose metabolism

Mesh:

Substances:

Year:  2017        PMID: 28764930     DOI: 10.1016/j.neurobiolaging.2017.06.016

Source DB:  PubMed          Journal:  Neurobiol Aging        ISSN: 0197-4580            Impact factor:   4.673


  33 in total

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