Higher education is not associated with greater cortical thickness in brain areas related to literacy or intelligence in normal aging or mild cognitive impairment

Abstract

Education may reduce risk of dementia through passive reserve, by increasing neural substrate. We tested the hypotheses that education is associated with thicker cortex and reduced rates of atrophy in brain regions related to literacy and intellectual ability. Healthy older adults and those with mild cognitive impairment were categorized into high (≥18 years) and low (≤13 years) education groups. Higher education was associated with thinner cortices in several areas, but one-year atrophy rates in these areas did not differ by education group. These results do not support a passive reserve model in which early-life education protects against dementia by increasing cortical thickness. Connectivity and synaptic efficiency or other lifestyle factors may more directly reflect cognitive reserve.

Keywords:

• Brain reserve
• Cortical thickness
• Education
• Literacy
• Hippocampal volume
• Mild cognitive impairment
• Aging

Acknowledgements

Data collection and sharing for this project were funded by the Alzheimer's Disease Neuroimaging Initiative (ADNI; National Institutes of Health Grant U01 AG024904). ADNI is funded by the National Institute on Aging, by the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: Abbott, AstraZeneca AB, Bayer Schering Pharma AG, Bristol-Myers Squibb, Eisai Global Clinical Development, Elan Corporation, Genentech, GE Healthcare, GlaxoSmithKline, Innogenetics, Johnson and Johnson, Eli Lilly and Co., Medpace, Inc., Merck and Co., Inc., Novartis AG, Pfizer Inc., F. Hoffman-La Roche, Schering-Plough, and Synarc, Inc., as well as nonprofit partners the Alzheimer's Association and Alzheimer's Drug Discovery Foundation, with participation from the U.S. Food and Drug Administration. Private sector contributions to ADNI are facilitated by the Foundation for the National Institutes of Health (www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer's Disease Cooperative Study at the University of California, San Diego. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of California, Los Angeles. This research was also supported by National Institutes of Health (NIH) Grants P30 AG010129, P50 AG05131, K01 AG030514, AG031224, and K01AG029218 and the National Center for Research Resources (U24 RR021382) and the Dana Foundation. J.P. received funding from a Veterans Administration Fellowship. Disclosures: A.M.D. is a founder of and holds equity interest in CorTechs Labs, Inc., La Jolla, CA, and serves on its Scientific Advisory Board. The terms of this arrangement have been reviewed and approved by the University of California, San Diego, CA, in accordance with its conflict of interest policies. The spouse of L.K.M. is president of CorTechs Labs, Inc., La Jolla, CA. The rest of the authors have no competing interests to declare.

Notes

Data used in preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (www.loni.ucla.edu/ADNI). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.ucla.edu/wp-content/uploads/how_to_apply/ADNI_Authorship_List.pdf