Purpose: As dual-phase amyloid-PET can evaluate amyloid (A) and neurodegeneration (N) with a single tracer injection, dual-phase tau-PET might be able to provide both tau (T) and N. Our study aims to assess the association of early-phase tau-PET scans and F-fluorodeoxyglucose (FDG) PET and their comparability in discriminating Alzheimer's disease (AD) patients and differentiating neurodegenerative patterns.
Methods: 58 subjects evaluated at the Geneva Memory Center underwent dual-phase F-Flortaucipir-PET with early-phase acquisition (eTAU) and F-FDG-PET within 1 year.
Introduction: The Next Move in Movement Disorders (NEMO) study is an initiative aimed at advancing our understanding and the classification of hyperkinetic movement disorders, including tremor, myoclonus, dystonia, and myoclonus-dystonia. The study has two main objectives: (a) to develop a computer-aided tool for precise and consistent classification of these movement disorder phenotypes, and (b) to deepen our understanding of brain pathophysiology through advanced neuroimaging techniques. This protocol review details the neuroimaging data acquisition and preprocessing procedures employed by the NEMO team to achieve these goals.
View Article and Find Full Text PDFThe goal of this paper is to build an automatic way to interpret conclusions from brain molecular imaging reports performed for investigation of cognitive disturbances (FDG, Amyloid and Tau PET) by comparing several traditional machine learning (ML) techniques-based text classification methods. Two purposes are defined: to identify positive or negative results in all three modalities, and to extract diagnostic impressions for Alzheimer's Disease (AD), Fronto-Temporal Dementia (FTD), Lewy Bodies Dementia (LBD) based on metabolism of perfusion patterns. A dataset was created by manual parallel annotation of 1668 conclusions of reports from the Nuclear Medicine and Molecular Imaging Division of Geneva University Hospitals.
View Article and Find Full Text PDFIncreasing evidence shows that neuroinflammation is a possible modulator of tau spread effects on cognitive impairment in Alzheimer's disease. In this context, plasma levels of the glial fibrillary acidic protein (GFAP) have been suggested to have a robust association with Alzheimer's disease pathophysiology. This study aims to assess the correlation between plasma GFAP and Alzheimer's disease pathology, and their synergistic effect on cognitive performance and decline.
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