Neurobiology of Aging
Volume 29, Issue 3 , Pages 329-340, March 2008

Accelerated age-related cortical thinning in healthy carriers of apolipoprotein E ɛ4

  • Thomas Espeseth

      Affiliations

    • Department of Psychology, University of Oslo, P.O. Box 1094, Blindern, N-0317 Oslo, Norway
    • Corresponding Author InformationCorresponding author. Tel.: +47 22845135; fax: +47 22845096.
    • ,
  • Lars T. Westlye

      Affiliations

    • Department of Psychology, University of Oslo, P.O. Box 1094, Blindern, N-0317 Oslo, Norway
    • ,
  • Anders M. Fjell

      Affiliations

    • Department of Psychology, University of Oslo, P.O. Box 1094, Blindern, N-0317 Oslo, Norway
    • ,
  • Kristine B. Walhovd

      Affiliations

    • Department of Psychology, University of Oslo, P.O. Box 1094, Blindern, N-0317 Oslo, Norway
    • ,
  • Helge Rootwelt

      Affiliations

    • Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway
    • ,
  • Ivar Reinvang

      Affiliations

    • Department of Psychology, University of Oslo, P.O. Box 1094, Blindern, N-0317 Oslo, Norway

Received 19 May 2006; received in revised form 24 October 2006; accepted 30 October 2006. published online 12 December 2006.

Abstract 

Effects of APOE genotype on age-related slopes of cortical thinning was estimated by measuring the thickness of the cerebral cortex on a point-by-point basis across the cortical mantle in 96 healthy non-demented volunteers aged 48–75 years. Fifty nine were APOE ɛ4− (no ɛ4 allele) and 37 were ɛ4+ (1 or 2 ɛ4 alleles). The genotype groups had similar age, sex and IQ. Two T1-weighted MP-RAGE sequences were averaged for each participant to yield images with high signal-to-noise ratio, and quantified using semi-automated analysis tools. ɛ4 carriers had thicker cortex than non-carriers in several frontal and temporal areas in both hemispheres, but showed a steeper age-related decline in adjacent areas. Upon comparison of the ɛ4-specific age-related thinning with previously published patterns of thinning in normal aging and Alzheimer's disease (AD), we conclude that APOE ɛ4 may function to accelerate thinning in areas found to decline in aging (medial prefrontal and pericentral cortex), but also to initiate thinning in areas associated with AD and amyloid-β aggregation (occipitotemporal and basal temporal cortex).

Keywords: Apolipoprotein E, Cortical morphometry, Brain aging, Individual differences, Alzheimer's disease

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PII: S0197-4580(06)00403-9

doi:10.1016/j.neurobiolaging.2006.10.030

Neurobiology of Aging
Volume 29, Issue 3 , Pages 329-340, March 2008

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