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Clinical Trial Summary

The reason why each specific degenerative disease is characterized by a different FDG PET pattern is still unclear today. There are four main hypotheses proposed to explain this selective vulnerability: 1) Nodal stress, theory according to which the main nodes of specific brain networks undergo wear and tear, 2) trans-neuronal diffusion, theory according to which some toxic agents/proteins or altered propagate along network connections through "Prion-like" mechanisms, 3) trophic failure, in which the interruption of inter-modal connectivity causes the loss of collateral trophic factors, and finally 4) shared vulnerability in which regions also distant from each other are part of a common network which gives a susceptibility uniformly distributed throughout the network. FDG PET provides in-vivo information on the distribution of brain synaptic dysfunction prior to complete neural death, and represents the main in vivo biomarker of neural dysfunction associated with different clinical conditions characterized by neurodegeneration phenomena. For this reason, FDG PET is considered a fundamental approach to shed light on the causes of selective brain vulnerability in various pathological conditions.


Clinical Trial Description

n/a


Study Design


Related Conditions & MeSH terms


NCT number NCT06180213
Study type Observational
Source IRCCS San Raffaele
Contact
Status Completed
Phase
Start date October 1, 2015
Completion date December 31, 2019

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