EVs in neurodegenerative diseases

Several studies have shown that in pathological conditions, circulating EV levels and chargo vary significantly compared to healthy individuals. For example, in Alzheimer’s disease (AD), it has been found that amyloid-beta and hyperphosphorylated tau are released from EVs, and their protein components can distinguish between mild cognitive impairment and AD. The main objectives of this longitudinal project are: 1) to characterize the molecular cargo of the circulating vesicular components in neurodegenerative diseases. 2) to verify the possibility of specific molecular profile/s that characterizes and distinguish each disease from another. 3) to identify any common molecular profiles that allow us to trace new pathogenetic pathways associated with neurodegeneration and related processes (e.g., inflammation). 4) to identify critical molecular hubs, whether common or specific to each disease, for further investigation, including for therapeutic purposes.