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. 2015;46(2):351-64.
doi: 10.3233/JAD-142292.

Mapping the Progression of Atrophy in Early- and Late-Onset Alzheimer's Disease

Mapping the Progression of Atrophy in Early- and Late-Onset Alzheimer's Disease

Raffaella Migliaccio et al. J Alzheimers Dis. 2015.

Abstract

The term early-onset Alzheimer's disease (EOAD) identifies patients who meet criteria for AD, but show onset of symptoms before the age of 65. We map progression of gray matter atrophy in EOAD patients compared to late-onset AD (LOAD). T1-weighted MRI scans were obtained at diagnosis and one-year follow-up from 15 EOAD, 10 LOAD, and 38 age-matched controls. Voxel-based and tensor-based morphometry were used, respectively, to assess the baseline and progression of atrophy. At baseline, EOAD patients already showed a widespread atrophy in temporal, parietal, occipital, and frontal cortices. After one year, EOAD had atrophy progression in medial temporal and medial parietal cortices. At baseline, LOAD patients showed atrophy in the medial temporal regions only, and, after one year, an extensive pattern of atrophy progression in the same neocortical cortices of EOAD. Although atrophy mainly involved different lateral neocortical or medial temporal hubs at baseline, it eventually progressed along the same brain default-network regions in both groups. The cortical region showing a significant progression in both groups was the medial precuneus/posterior cingulate.

Keywords: Age of onset; Alzheimer’s disease; atrophy progression; default mode network; tensor based morphometry; voxel based morphometry.

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Figures

Figure 1
Figure 1
The figure shows grey matter (GM) atrophy at baseline (on the top; p< 0.05 FWE) and atrophy progression after one year (at the bottom) in early onset (EOAD) Alzheimer’s disease patients compared with matched healthy controls. Results are displayed on the Montreal Neurological Institute (MNI) template available on MRIcron software (http://www.mccauslandcenter.sc.edu/mricro/mricron/). Color bars denote T values (on the top) and percentage of GM reduction during follow up (at the bottom).
Figure 2
Figure 2
The figure shows grey matter (WM) atrophy at baseline (on the top; p< 0.001 uncorrected) and atrophy progression after one year (at the bottom) in late onset (LOAD) Alzheimer’s disease patients compared with matched healthy controls. Results are displayed on the Montreal Neurological Institute (MNI) template available on MRIcron software (http://www.mccauslandcenter.sc.edu/mricro/mricron/). Color bars denote T values (on the top) and percentage of GM reduction during follow up (at the bottom).
Figure 3
Figure 3
Common and specific patterns of atrophy at baseline in EO and LOAD patients. Common area (blue) is centered on left hippocampus (conjunction analysis). More severe atrophy in EOAD (red) vs. LOAD were found in the lateral inferior and superior parietal regions, and occipital lobes bilaterally, as well as left posterior temporal and left fusiform areas. No specific areas of atrophy were found for LOAD.
Figure 4
Figure 4
Common and specific patterns of atrophy progression in EO and LOAD patients. Common area (blue) is centered on precuneus and posterior cingulum (conjunction analysis). More severe atrophy progression in EOAD (red) vs. LOAD were found in lateral and medial frontal areas, cingulate gyrus, lateral temporal regions as well as in peri-central regions, such the post-central gyrus, and the supplementary motor areas. LOAD patients (green) showed a greater atrophy progression in ventral frontal and temporal regions, included parahippocampal and fusiform gyri, as well as in lateral frontal and temporal, and occipital regions.

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