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Neuroimage Clin. 2013 Sep 16;3:352-60. doi: 10.1016/j.nicl.2013.09.001. eCollection 2013.

The diffeomorphometry of temporal lobe structures in preclinical Alzheimer's disease.

Author information

  • 1Center for Imaging Science, Johns Hopkins University, Baltimore, MD 21218, USA ; Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD 21218, USA ; Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21218, USA.
  • 2Center for Imaging Science, Johns Hopkins University, Baltimore, MD 21218, USA ; Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD 21218, USA ; Department of Applied Mathematics and Statistics, Johns Hopkins University, Baltimore, MD 21218, USA.
  • 3Center for Imaging Science, Johns Hopkins University, Baltimore, MD 21218, USA.
  • 4Center for Imaging Science, Johns Hopkins University, Baltimore, MD 21218, USA ; Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21218, USA.
  • 5Department of Biostatistics, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, MD 21205, USA.
  • 6Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
  • 7Department of Neurology, Johns Hopkins Bayview Medical Center, Baltimore, MD 21205, USA.
  • 8Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Abstract

This paper examines morphometry of MRI biomarkers derived from the network of temporal lobe structures including the amygdala, entorhinal cortex and hippocampus in subjects with preclinical Alzheimer's disease (AD). Based on template-centered population analysis, it is demonstrated that the structural markers of the amygdala, hippocampus and entorhinal cortex are statistically significantly different between controls and those with preclinical AD. Entorhinal cortex is the most strongly significant based on the linear effects model (p < .0001) for the high-dimensional vertex- and Laplacian-based markers corresponding to localized atrophy. The hippocampus also shows significant localized high-dimensional change (p < .0025) and the amygdala demonstrates more global change signaled by the strength of the low-dimensional volume markers. The analysis of the three structures also demonstrates that the volume measures are only weakly discriminating between preclinical and control groups, with the average atrophy rates of the volume of the entorhinal cortex higher than amygdala and hippocampus. The entorhinal cortex thickness also exhibits an atrophy rate nearly a factor of two higher in the ApoE4 positive group relative to the ApoE4 negative group providing weak discrimination between the two groups.

PMID:
24363990
PMCID:
PMC3863771
DOI:
10.1016/j.nicl.2013.09.001
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