Publications by authors named "G Vanderlinden"
Introduction: The longitudinal progression of synaptic loss in Alzheimer's disease (AD) and how it is affected by tau pathology remains poorly understood.
Methods: Thirty patients with amnestic mild cognitive impairment (aMCI) and 26 healthy controls underwent cognitive evaluations and tau, synaptic vesicle protein 2A (SV2A), and amyloid positron emission tomography. Twenty-one aMCI underwent 2-year follow-up (FU) investigations.
Background: Neuronal hyperexcitability has been proposed to play a key role in Alzheimer's disease (AD). Understanding the relation between this enhanced excitability and AD pathology could provide a window for therapeutic interventions. However epileptiform activity is often subclinical, hidden on scalp EEG and very challenging to assess with current diagnostic modalities.
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- An SVM-based method was developed to establish pseudo-reference regions in brain PET scans, aimed at minimizing variability across scans and subjects.
- The method utilized PET datasets from various groups to train a classifier and identify key brain regions for classification, which were tested in three different cohorts using distinct PET tracers.
- Results showed that the cerebellum, brainstem, subcortical white matter, and temporal cortex consistently emerged as pseudo-reference regions, indicating the approach's reliability even with fewer subjects and across different tracers.
Objective: To investigate whether tau accumulation is higher in late life depression (LLD) compared to non-depressed cognitively unimpaired (CU) older adults. To situate these findings in the neurodegeneration model of LLD by assessing group differences in tau and grey matter volume (GMV) between LLD, non-depressed CU and mild cognitive impairment due to Alzheimer's Disease (MCI).
Design: Monocentric, cross-sectional study.
Both sleep alterations and epileptiform activity are associated with the accumulation of amyloid-β and tau pathology and are currently investigated for potential therapeutic interventions in Alzheimer's disease (AD). However, a bidirectional intertwining relation between sleep and neuronal hyperexcitability might modulate the effects of AD pathology on the corresponding associations. To investigate this, we performed multiple day simultaneous foramen ovale (FO) plus scalp EEG and polysomnography (PSG) recordings and acquired 18F-MK6240 tau PET-MR in three patients in the prodromal stage of AD and in two patients with mild and moderate dementia due to AD, respectively.
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