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P2–198: The ROSAS study: Baseline MRI characteristics
Author(s) -
Bracoud Luc,
Lala Françoise,
Bonneville Fabrice,
Pueyo Maria,
Gouttard Sylvain,
Guignot Isabelle,
Sastre Nathalie,
Ousset PierreJean,
Pachai Chahin,
Vellas Bruno
Publication year - 2013
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2013.05.843
Subject(s) - medicine , dementia , neuropsychology , cognitive impairment , audiology , cognition , disease , psychiatry
to investigate potential differences in grey matter (GM) volume between FAD and early onset SAD (EO-SAD) patients. Methods: 20 healthy controls, 22 FAD and 24 EO-SAD patients were recruited from an AD research study at the Dementia Research Centre. (See Table 1 for demographics). Volumetric T1 weighted MRI scans were acquired and maps of GM volume produced using the VBM8 toolbox of SPM. Three FAD subjects were excluded due to poor segmentations caused by severe motion artefacts or white matter disease. The GMmaps were then spatially normalized to a groupwise template of the remaining participants. During the normalization, the maps were modulated to conserve tissue volume. Voxelwise modeling of differences in smoothed (Full Width Half Max1⁄46mm) GM maps was performed using a three-level group factor (Control, FAD, EO-SAD), controlling for age, gender, and total intracranial volume. Statistical maps were generated using permutation testing (n1⁄410,000) with correction for multiple comparisons using threshold free cluster enhancement and variance smoothing of 3mm to control Family Wise Error (FWE) at p<0.05. Results: Significant findings (FWE corrected, p<0.05) are shown between controls and the two AD groups in the Figure. There were widespread decreases in GM observed in both EO-SAD and FAD when compared to controls, particularly involving the precuneus, temporal lobe, cingulate gyrus, caudate, putamen, and thalamus. No significant differences between FAD and EO-SAD survived correction for multiple comparisons (see bottom row of the Figure). This is further illustrated in the third row of the Figure, where superimposing the two results shows similar atrophy patterns. Conclusions: This analysis provides no evidence of distinct GM atrophy patterns for FAD and EO-SAD. Differences may still exist, and further analysis will incorporate additional subjects and include sensitive volumetric and longitudinal measures in key structures. Importantly, comparison of atrophy patterns with a late onset SAD group will also be made.