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Age-Related Changes in the Thickness of Cortical Zones in Humans

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Abstract

Structural neuroimaging studies have demonstrated that all regions of the cortex are not affected equally by aging, with frontal regions appearing especially susceptible to atrophy. The “last in, first out” hypothesis posits that aging is, in a sense, the inverse of development: late-maturing regions of the brain are preferentially vulnerable to age-related loss of structural integrity. We tested this hypothesis by analyzing age-related changes in regional cortical thickness via three methods: (1) an exploratory linear regression of cortical thickness and age across the entire cortical mantle (2) an analysis of age-related differences in the thickness of zones of cortex defined by functional/cytoarchitectural affiliation (including primary sensory/motor, unimodal association, heteromodal association, and paralimbic zones), and (3) an analysis of age-related differences in the thickness of regions of cortex defined by surface area expansion in the period between birth and early adulthood. Subjects were grouped as young (aged 18–29, n = 138), middle-aged (aged 30–59, n = 80), young-old (aged 60–79, n = 60), and old–old (aged 80+, n = 38). Thinning of the cortex between young and middle-aged adults was greatest in heteromodal association cortex and regions of high postnatal surface area expansion. In contrast, thinning in old–old age was greatest in primary sensory/motor cortices and regions of low postnatal surface area expansion. In sum, these results lead us to propose a sequential “developmental-sensory” model of aging, in which developmental factors influence cortical vulnerability relatively early in the aging process, whereas later—in more advanced stages of aging—factors specific to primary sensory and motor cortices confer vulnerability. This model offers explicitly testable hypotheses and suggests the possibility that normal aging may potentially allow for multiple opportunities for intervention to promote the structural integrity of the cerebral cortex.

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Acknowledgment

This study was supported by grants from the NIA R01-AG29411, R21-AG29840, P50-AG005134, and NCRR P41-RR14075, U24-RR021382, Harvard NeuroDiscovery Center, and the Alzheimer’s Association.

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Authors and Affiliations

  1. Frontotemporal Dementia Unit, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

    Scott M. McGinnis, Michael Brickhouse, Belen Pascual & Bradford C. Dickerson

  2. Departments of Neurology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

    Scott M. McGinnis & Bradford C. Dickerson

  3. Departments of Psychiatry, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

    Michael Brickhouse & Bradford C. Dickerson

  4. Massachusetts Alzheimer’s Disease Research Center, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

    Scott M. McGinnis & Bradford C. Dickerson

  5. Division of Cognitive and Behavioral Neurology, Department of Neurology, Brigham & Women’s Hospital, 221 Longwood Avenue, Boston, MA, 02115, USA

    Scott M. McGinnis

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  1. Scott M. McGinnis
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Correspondence to Scott M. McGinnis.

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McGinnis, S.M., Brickhouse, M., Pascual, B. et al. Age-Related Changes in the Thickness of Cortical Zones in Humans. Brain Topogr 24, 279–291 (2011). https://doi.org/10.1007/s10548-011-0198-6

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  • DOI: https://doi.org/10.1007/s10548-011-0198-6

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