ORCID Profile
0000-0001-5862-640X
Current Organisation
KU Leuven
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Publisher: MDPI AG
Date: 07-06-2023
Abstract: In the original publication [...]
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 03-06-2020
DOI: 10.1212/WNL.0000000000009818
Abstract: To investigate in vivo whether synaptic loss and neurofibrillary tangle load spatially overlap and correlate with clinical symptoms in patients with amnestic mild cognitive impairment (aMCI). In this cross-sectional study, 10 patients with aMCI and 10 healthy controls underwent triple PET-MRI with 11 C-UCB-J (synaptic vesicle protein 2A), 18 F-MK-6240 (tau deposition), and 11 C-Pittsburgh compound B (β-amyloid) and neuropsychological assessment. Gray matter atrophy was assessed by voxel-based morphometry with T1-weighted MRIs. Voxel-wise and volume-of-interest analyses were conducted on PET data. The interrelationship of synaptic density and tau deposition was investigated. We also investigated correlations of 18 F-MK-6240 and 11 C-UCB-J binding with cognitive performance. Compared to controls, patients with aMCI showed a decreased 11 C-UCB-J binding mainly in substructures of the medial temporal lobe (MTL 48%–51%, p cluster = 0.02). Increased 18 F-MK6240 binding in the same region was observed (42%–44%, p cluster = 0.0003), spreading to association cortices. In the MTL, higher 18 F-MK-6240 binding inversely related to lower 11 C-UCB-J binding ( p = 0.02, r = −0.76). Decreased performance on cognitive tests was associated with both increased 18 F-MK-6240 and decreased 11 C-UCB-J binding in the hippoc us ( p 0.01, r 0.7), although in a multivariate analysis only 18 F-MK-6240 binding was significantly related to cognitive performance. Patients with aMCI have high tau deposition and synaptic density loss mainly in key regions known to be involved in early cognitive impairment, indicating that these are interrelated in the MTL, while tau binding had already spread toward association cortices. Longitudinal data are needed to provide further insight into the temporal aspects of this relationship.
Publisher: MDPI AG
Date: 18-03-2023
Abstract: Amyotrophic lateral sclerosis (ALS) is characterized by progressive loss of upper and lower motor neurons. In 10% of patients, the disorder runs in the family. Our aim was to study the impact of ALS-causing gene mutations on cerebral glucose metabolism. Between October 2010 and October 2022, 538 patients underwent genetic testing for mutations with strong evidence of causality for ALS and 18F-2-fluoro-2-deoxy-D-glucose-PET (FDG PET), at University Hospitals Leuven. We identified 48 C9orf72-ALS and 22 SOD1-ALS patients. After propensity score matching, two cohorts of 48 and 21 matched sporadic ALS patients, as well as 20 healthy controls were included. FDG PET images were assessed using a voxel-based and volume-of-interest approach. We observed widespread frontotemporal involvement in all ALS groups, in comparison to healthy controls. The degree of relative glucose metabolism in SOD1-ALS in motor and extra-motor regions did not differ significantly from matched sporadic ALS patients. In C9orf72-ALS, we found more pronounced hypometabolism in the peri-rolandic region and thalamus, and hypermetabolism in the medulla extending to the pons, in comparison to matched sporadic ALS patients. Our study revealed C9orf72-dependent differences in glucose metabolism in the peri-rolandic region, thalamus, and brainstem (i.e., medulla, extending to the pons) in relation to matched sporadic ALS patients.
No related grants have been discovered for Michel Koole.