Study of Cerebral Glucose Metabolism in Neurodegenerative Diseases and Head Trauma

Study of Cerebral Glucose Metabolism in Neurodegenerative Diseases and Head Trauma: Retrospective Review of an Large Cohort of FDG PET Data

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.

Inclusion Criteria:

• presence of diagnosis of neurodegenerative disease.

Exclusion Criteria:

• patients< 18 years