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P1‐360: Association of disease severity with VBM measured reduced regional gray matter volumes in Alzheimer's disease patients
Author(s) -
Huang Qiu,
Wang Tao,
Chen Kewei,
Reiman Eric,
Xiao Shifu
Publication year - 2011
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.2011.05.640
Subject(s) - precuneus , cuneus , statistical parametric mapping , voxel based morphometry , voxel , lingual gyrus , dementia with lewy bodies , spatial normalization , grey matter , magnetic resonance imaging , posterior cingulate , occipital lobe , medicine , superior frontal gyrus , fusiform gyrus , psychology , audiology , neuroscience , white matter , dementia , pathology , radiology , disease , cognition
AD offspring), we can assess the earliest cortical changes associated with AD.Methods:MR scans were collected from 140 cognitively healthy participants, 71 AD offspring and 69 non-AD offspring. Additionally, blood was drawn for ApoE genotyping. MRI data were processed using FreeSurfer. Primary analyses examined family history and ApoeE4 effects on cortical thickness. Secondary analyses examined age effects within groups. All comparisons were adjusted using False Discovery Rate at a significance threshold of p< 0.05. Statistical surface maps were generated using general linear models. Intensity of displayed values is based on a -log(10)p relationship. Results: There were no statistically significant differences between family history and ApoE4 groups. Within AD offspring, cortical thickness and age correlations yielded large areas of statistically significant negative correlations in precuneus, superior frontal and superior temporal gyri (bilaterally), indicating increasing age is related to decreasing cortical thickness (i.e. atrophy). Within non-AD offspring, we observed similar correlations in small regions of superior temporal, insula and lingual cortices. Within maternal AD offspring, similar aging-related cortical atrophy patterns as abovewere found, that was absent in paternal AD offspring. Also, late-onset AD offspring (&> 60 years) showed similar aging-related cortical atrophy pattern as above, that was absent in early-onset AD offspring. See Figure. Conclusions: The lack of group differences in primary analyses is not unexpected. Research indicates the ApoE4 allele is implicated in late-onset AD; therefore no effect should be observed. Within AD offspring, we found aging-related cortical thinning in regions AD is known to affect.Within nonAD offspring, we found different patterns of aging-related cortical thinning that may be the effect of normal aging. Results suggest that as AD offspring age, cortical atrophy is more prominent, particularly if the parent with AD is the mother or of late-onset.