4.7 Article

Longitudinal changes in medial temporal cortical thickness in normal subjects with the APOE-4 polymorphism

期刊

NEUROIMAGE
卷 53, 期 1, 页码 37-43

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.neuroimage.2010.06.009

关键词

Alzheimer's disease; APOE genotype; High-resolution MRI; Medial temporal lobe; Cortical unfolding; Cortical thickness

资金

  1. Abbott
  2. Brainstorming Co.
  3. Dakim
  4. Eisai
  5. Forest
  6. Myriad Genetics
  7. Novartis
  8. Ortho-McNeil
  9. Pfizer
  10. Radica
  11. Siemens
  12. Medivation
  13. Alzheimer's Association Speakers Bureau
  14. Keiro Senior Health Services
  15. NIH [P01-AG025831, AG13308, P50 AG 16570, MH/AG58156, MH52453, AG10123, M01-RR00865]
  16. General Clinical Research Centers Program
  17. Fran and Ray Stark Foundation Fund
  18. Larry L. Hillblom Foundation
  19. Max Kade Foundation

向作者/读者索取更多资源

People with the apolipoprotein-E epsilon 4 (APOE-4) genetic risk for Alzheimer's disease show morphologic differences in medial temporal lobe regions when compared to non-carriers of the allele. Using a high-resolution MRI and cortical unfolding approach, our aim was to determine the rate of cortical thinning among medial temporal lobe subregions over the course of 2 years. We hypothesized that APOE-4 genetic risk would contribute to longitudinal cortical thickness change in the subiculum and entorhinal cortex, regions preferentially susceptible to Alzheimer's disease related pathology. Thirty-two cognitively intact subjects, mean age 61 years, 16 APOE-4 carriers, 16 non-carriers, underwent baseline and follow-up MRI scans. Over this relatively brief interval, we found significantly greater cortical thinning in the subiculum and entorhinal cortex of APOE-4 carriers when compared to non-carriers of the allele. Average cortical thinning across all medial temporal lobe subregions combined was also significantly greater for APOE-4 carriers. This finding is consistent with the hypothesis that carrying the APOE-4 allele renders subjects at a higher risk for developing Alzheimer's disease. (C) 2010 Elsevier Inc. All rights reserved.

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