Impact of Microglial Activation on Synaptic Density in Alzheimer's Disease
This study aims to analyse, in vivo, the interplay between microglial activation and tau pathology in Alzheimer's disease (AD) using \[18F\]-DPA-714 and \[18F\]-Ro948 tracers by Position Emission Tomography (PET), and their consequences on synaptic density using \[11C\]-UCB-J, a recent PET radioligand. By coupling advanced neuroimaging techniques in AD patients, while comparing them to controls, we will be able to study, for the first time in humans, the interaction between neuroinflammation, tau pathology, synaptic density, and their impact on AD progression. Joint analyses of peripheral immune biomarkers, carried out as a secondary objective, will further aim at defining peripheral correlates of this interplay. Overall, we aim to refine AD subgroup classification in order to improve and to refine the design of new therapeutic trials.
• Adult (older than 18 years)
• Women old enough to procreate under effective contraception
• Signed consent
• Absence of general or systemic disorders that may interfere with cognition.
• Progressive amnestic syndrome, associated or not with other cognitive impairments,
• CDR = 0.5 or 1
• Absence of general or systemic disorders that may interfere with cognition or PET imaging analysis,
• Absence of brain lesions as determined by MRI carried out within the framework of usual care.
• Presence of CSF biomarkers profile suggestive of AD
• absence of subjective problems with memory and normal scores on the MMSE (MMSE \> 27) with no more than one word missing.
• older than 50 years old.
• Scores on the Free and Cued Selective Reminding Test (FCSRT) of \>25 for free recall and \>44 for total recall.
• absence of general or systemic disorders that may interfere with cognition at follow-up.
⁃ Controls will be matched to AD patients for age and education level.