Densité des dépôts de la protéine Tau versus activité métabolique cortico-cérébrale chez des patients atteints de maladie d’Alzheimer ou de pathologies apparentées

Abstract

IntroductionThe extracellular deposits of major senile plaques composed of Aβ proteins and intracellular degenerations or neurofibrillary degenerations (NFD) made up of hyperphosphorylated tau proteins are characteristic of Alzheimer's disease (AD). These characteristic lesions develop well before the first symptoms. NFD lesions seem to correlate with clinical symptomatology and allow Alzheimer's disease to be classified into neuropathological stages. In this study, we wanted to compare metabolic activity and NFD density by molecular imaging in a small cohort of subjects. Materials and methodsIn this study we evaluated the binding profile (brain density and distribution) of tau aggregates using [18F] – AV-1451 ([18F] -T807 or flortaucipir) PET in a group of 7 patients with clinical diagnosis of AD or related neurodegenerative pathology but with a very variable evolutionary profile (MMS between 15 and 25). All subjects also underwent a [18F] – FDG PET scan to assess their neuronal metabolic activity. For each subject, [18F] – T807 binding intensity and degree of hypometabolism were visually quantified in 5 levels for each predefined cortical region. ResultsFour subjects had a hypometabolic pattern supporting their diagnosis and which, moreover, was consistent with the distribution of NFD, however with slightly more extensive NFD lesions, particularly in the occipital region. One subject had neither hypometabolism nor a significant NFD array. One subject had predominantly hypometabolism in the frontotemporal cortex without significant lesion of DNF. The 7th subject presented diffuse cortical hypometabolism with few NFD lesions. ConclusionDespite a limited number of subjects, results seem to confirm the close link between the presence of the NFD lesions visible on tau PET imaging and neurodegeneration in AD.