Premium
P1‐102: Changes in cortical thickness in asymptomatic individuals at genetic risk for Alzheimer's disease
Author(s) -
Bassett Susan S.,
Bazin PierreLouis,
Cristinzio Catherine,
Pham Dzung L.
Publication year - 2009
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.2009.04.107
Subject(s) - parahippocampal gyrus , asymptomatic , temporal lobe , cognition , medicine , parietal lobe , neuroscience , neuroimaging , psychology , audiology , cardiology , pathology , epilepsy
Background: The identification of preclinical markers for Alzheimer’s disease (AD) is vital for understanding etiology and targeting potential treatments. Our group is focused on this issue and has been studying asymptomatic individuals over the age of 50 who are at genetic risk for AD, (being the offspring of autopsied AD cases and from families with multiple affected first-degree relatives). The recent development of techniques to measure the thickness of the cortical mantle using MRI images provides another means to potentially identify structural brain changes that precede the clinical diagnosis of AD. Methods: 197 (100 at-risk; 97 controls) were enrolled in a longitudinal study which included laboratory work, cognitive testing and both structural and functional MRI. Individuals were seen twice, three years apart. Participants were imaged at each time point on the same 1.5 T magnet. Images for structural measurements are acquired with a high resolution anatomical image of the brain obtained using a T1-weighted, 3D MP-RAGE sequence. The automated CRUISE (Cortical Reconstruction Using Implicit Surface Evolution) method was used to reconstruct the cerebral cortex and compute average cortical thickness for the temporal, parietal and frontal lobes, as well as specific temporal structures, including the parahippocampal gyrus. Results: Inspection of Time 2 cognitive testing data found 13 individuals had declined and met criteria for Mild Cognitive Impairment (MCI). Analysis of cortical thickness measurements found those who declined cognitively had significant thinning of the left temporal lobe (t1⁄42.48, p<.05), right frontal lobe (t1⁄42.44, p<.05) and parahippocampal gyrus (PHG) (t1⁄42.49, p<.05). Voxel based morphometric analysis revealed those who declined had at baseline significantly smaller volumes of the left frontal lobe and thalamus, bilaterally. Conclusions: Asymptomatic individuals at genetic risk for AD who progressed to MCI are characterized by cortical thinning of the left temporal and right frontal lobes as well as the parahippocampal gyrus. This extends previous work on cortical thinning to asymptomatic high risk individuals and illuminates the dissociation between volume loss and loss associated with the cortical mantle. Further work is needed to determine whether baseline characteristics or patterns of change prove the most valuable for predicting cognitive decline.