Premium
P1‐227: QUALITY ASSESSMENT OF RESTING‐STATE FUNCTIONAL MRI EXPERIMENTS IN CLINICAL TRIALS
Author(s) -
Marais Léa,
Lee Sarah,
Hill Derek,
McLeish Kate
Publication year - 2014
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.2014.05.466
Subject(s) - siemens , clinical trial , resting state fmri , neuroimaging , medical physics , computer science , quality (philosophy) , medicine , psychology , nuclear medicine , pathology , radiology , psychiatry , physics , quantum mechanics , philosophy , epistemology
Background: 18 F-FDG-PET is widely used in helping diagnose Alzheimer’s disease (AD) due to the localized decrease in brain glucose uptake, especially in the temporal and parietal cortex. Ketones are the brain’s principal non-glycolytic energy substrates. Our group developed a new brain ketone PET tracer, 11 C-acetoacetate (11 C-AcAc), to address the question: in mild AD, does regional brain ketone uptake reflect the same pattern of deteriorating brain glucose uptake? Methods: Cognitively healthy controls (n1⁄430, age 75 y) were compared to mild AD (n1⁄410, age 76 y). The clinical diagnosis of AD was made according to NINCDS-ADRDA criteria. Structural 1.5T MR and PET imaging with both 11 C-AcAc and 18 F-FDG were acquired for all participants. Dynamic PET images were co-registered to MR images and corrected for partial volume effect. Cerebral metabolic rates (CMR; mmol/100 g/min) for glucose (CMR glu) and ketones (CMR ket) were calculated. Group differences were examined using Mann Whitney U-tests with a multiple comparison correction set at 0.05. Results: Global CMR glu was 12% lower in AD compared to the healthy agematched controls (34.265.0 vs. 38.364.7 mmol/100g/min, respectively; P 1⁄4 0.033). Most of this difference was confined to the posterior cingulate, thalamus, angular and supramarginal gyri, and temporal cortex where CMR glu was 13-32% lower in AD (P 0.022). In contrast to brain glucose uptake, CMR ket was not different in AD vs. controls, either globally (0.3560.17 vs. 0.316 0.24mmol/100g/min, respectively; P1⁄4 0.379) or in any individual brain regions (P 0.173). In both controls and AD groups, CMR ket was positively correlated to plasma ketones (r1⁄4 +0.898 and r1⁄4 +0.865, respectively; P 0.001). Conclusions: Relative to cognitively-healthy agematched controls, regions of the brain with deteriorating glucose uptake in mild AD appear to have no problem taking up ketones. Our findings support the concept of using ketones as a potential complementary strategy to counteract brain energetic deficit and cognitive impairment in mild AD.