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P4‐199: Comparative Longitudinal Change of Functional Connectivity, Diffusion and Structural MRI Markers in a Prodromal/Mild Alzheimer’s Disease Population
Author(s) -
Slieker Lawrence,
Lin Qun,
Pinsard Basile,
Longo dos Santos Clarisse,
Wolz Robin,
Perlbarg Vincent,
Poupon Cyril,
Chevrette Antoine,
Martenyi Ferenc,
Dubois Bruno,
Mangin Jean-Francois,
Hill Derek L.,
Schwarz Adam J.
Publication year - 2016
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.2016.06.2291
Subject(s) - diffusion mri , white matter , default mode network , resting state fmri , dementia , medicine , population , episodic memory , cardiology , clinical dementia rating , fractional anisotropy , corpus callosum , psychology , nuclear medicine , magnetic resonance imaging , neuroscience , functional connectivity , disease , radiology , cognition , environmental health
eal, QC, Canada; Montreal Neurological Institute, Montreal, QC, Canada; Universit e de Montr eal, Montr eal, QC, Canada; 9 Centre for Studies on Prevention of Alzheimer’s Disease (StoP-AD Centre), Douglas Mental Health Institute, Verdun, QC, Canada. Contact e-mail: tharick.alipascoal@mail.mcgill.ca Background: Although individuals presenting abnormalities of both amyloid-b (Ab) deposition and neuronal injury are especially vulnerable to disease progression, the regional association of these two pathologies as a determinant of cognitive decline remains unclear. Here, we tested, at voxel level, whether co-localized interactions between abnormal Ab and brain hypometabolism determine subsequent cognitive decline in individuals with mild cognitive impairment (MCI).Methods:In order to test this framework, we assessed 309 amnesticMCI individuals formADNI cohort who underwent [F]florbetapir and [F]FDG positron emission tomography (PET) at baseline and a general cognitive performance testing (mini-mental state examination (MMSE)) at baseline and at 2-year follow-up visits (Table 1). First, cut-off analysis at every voxel was performed for both ligands, contrasting cognitively normal (n1⁄4209) and Alzheimer’s disease (AD) (n1⁄481) individuals, based on the best operating point of the receiver operating characteristic (ROC) curve. Second, parametrical maps of normality and abnormality at every voxel were generated for both ligands using the aforementioned cut-off maps for each MCI individual. Finally, using Voxel-stats, a voxel-based interaction model was built to assess the brain regions in which the coexistence of an abnormal [F]florbetapir and [F]FDG standardized uptake ratios (SUVR) interacted to determine an increased rate of cognitive decline over 2 years, as described in the formula: DMMSE 1⁄4 b0 + b1(florbetapir SUVR (0,1)) + b2(FDG SUVR(0,1)) + b3(florbetapir SUVR (0,1)*FDG SUVR (0,1)) + covariates + error. The statistical parametric maps were adjusted for age, gender, education, APOE ε4 status, baselineMMSEand corrected formultiple testing at a threshold ofP< 0.05.Results:The voxel-based interactionmodel revealed that a synergistic effect between abnormal [F]florbetapir and [F]FDG SUVRs in the precuneus and posterior cingulate cortices determined a faster rate of cognitive decline in amnestic MCI individuals (P < 0.05) (Figure 1). Conclusions:Our results support the notion that the regional synergism between brain Ab and metabolic injury is associated with subsequent clinical progression in patients with MCI.