Affiliations: [a] Center for Imaging Science, Johns Hopkins University, Baltimore, MD, USA | [b] Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA | [c] Department of Radiology, University of California, San Diego, La Jolla, CA, USA | [d] Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD, USA | [e] Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA
Correspondence:
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Correspondence to: Xiaoying Tang, Center for Imaging Science, Johns Hopkins University, 301 Clark Hall, 3400N. Charles Street, Baltimore, MD 21218, USA. Tel.: +1 410 949 0497; Fax: +1 410 516 4594; xtang@cis.jhu.edu
Note: [1] Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (http://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in the analysis or writing of this report.
Abstract: This paper examines how age intervenes in the effects of APOE ɛ4 allele on the volume and shape morphometrics of the hippocampus and the amygdala in mild cognitive impairment (MCI) and Alzheimer’s disease. We evaluate the structural morphological differences between ɛ4 carriers and non-carriers in two age-dependent subgroups; younger than 75 years (Young-Old) and older than 80 years (Very-Old). While we show that the four structures of interest atrophy significantly in the ɛ4 carriers, relative to the non-carriers, of the Young-Old group, this effect is not observed in their Very-Old counterparts. The structures in the right hemisphere are found to be more affected by the APOE genotype than those in the left hemisphere and we identify the relevant regions in which significant atrophy occurs to be parts of the basolateral, centromedial, and lateral nucleus subregions of the amygdala and the CA1 and subiculum subregions of the hippocampus. We also observe that the APOE genotype only affects MCI patients that deteriorated to dementia within 3 years while leaving their “non-converting” counterparts unaffected.
Keywords: Age intervention, Alzheimer’s disease, amygdala, apolipoprotein E, conversion, hippocampus, mild cognitive impairment, shape morphometrics
