Published in:
01-02-2020 | Alzheimer's Disease | Original Article
In vivo imaging of synaptic loss in Alzheimer’s disease with [18F]UCB-H positron emission tomography
Authors:
Christine Bastin, Mohamed Ali Bahri, François Meyer, Marine Manard, Emma Delhaye, Alain Plenevaux, Guillaume Becker, Alain Seret, Christine Mella, Fabrice Giacomelli, Christian Degueldre, Evelyne Balteau, André Luxen, Eric Salmon
Published in:
European Journal of Nuclear Medicine and Molecular Imaging
|
Issue 2/2020
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Abstract
Purpose
Loss of brain synapses is an early pathological feature of Alzheimer’s disease. The current study assessed synaptic loss in vivo with positron emission tomography and an 18F-labelled radiotracer of the synaptic vesicle protein 2A, [18F]UCB-H.
Methods
Twenty-four patients with mild cognitive impairment or Alzheimer’s disease and positive [18F]Flutemetamol amyloid-PET were compared to 19 healthy controls. [18F]UCB-H brain uptake was quantified with Logan graphical analysis using an image-derived blood input function. SPM12 and regions-of-interest (ROI) analyses were used for group comparisons of regional brain distribution volumes and for correlation with cognitive measures.
Results
A significant decrease of [18F]UCB-H uptake was observed in several cortical areas (11 to 18% difference) and in the thalamus (16% difference), with the largest effect size in the hippocampus (31% difference). Reduced hippocampal uptake was related to patients’ cognitive decline (ROI analysis) and unawareness of memory problems (SPM and ROI analyses).
Conclusions
The findings thus highlight predominant synaptic loss in the hippocampus, confirming previous autopsy-based studies and a recent PET study with an 11C-labelled SV2A radiotracer. [18F]UCB-H PET allows to image in vivo synaptic changes in Alzheimer’s disease and to relate them to patients’ cognitive impairment.