Détails de la réservation
- Le : 3 November 2017
- De : 11 h 30
- à : 12 h 30
- Salle : Amphi Centre Broca Nouvelle - Aquitaine
Détails de l'évènement
Jérôme Badaut
PhD, CR1, CNRS,INCIA, Team: Brain Molecular Imaging.
Domain: Neurovascular unit physiology/ traumatic brain injury/ stroke/ edema/ astrocytes
"Gliovascular unit dysfunctions precede neuronal alterations after pediatric brain injury"
Résumé
Traumatic brain injury (TBI) is a major public health issue with at least one million-hospital admissions/year. Mild TBI is defined with a Glasgow coma score > 13, no or transient (< 30 min) loss of consciousness, no major alterations on CT scans and no apparent short-term cognitive deficits. It is now recognized that mild TBI causes significant early and long-term morbidity and is a risk factor for cognitive decline and dementia including Alzheimer Disease. Although TBI hits the pediatric population particularly hard, very little research has been carried out in juvenile models of TBI (jTBI), resulting in limited knowledge regarding its underlying pathophysiological mechanisms, a particularly alarming situation as these mechanisms are different between children and adults. It is critical to have a better understanding of the short- and long-term brain molecular changes in order to accurately develop new drug treatments that could minimize or prevent these long-term cognitive sequelae.
We previously demonstrated long-term grey matter (GM) changes in the blood-brain barrier (BBB) and neurovascular unit (NVU) after jTBI. However, as long-term white matter (WM) changes occur and have been implicated in accelerated cognitive decline in clinical and pre-clinical studies, we hypothesize that early post-jTBI vascular dysfunction with changes in NVU may significantly contribute to long-term WM and GM injury and resultant cognitive impairment.
Association between vessel changes and cognitive decline suggests that jTBI is a clear vascular contributor to cognitive impairment and dementia. Such early WM and GM pathophysiologic events are poorly understood and understudied in mild TBI, but likely initiate a downward spiral of events that continue for several weeks after injury known to impair the myelination process with long-term cognitive decline.
Definition of NVU and its importance in brain functions as well as pathophysiological changes will be discussed during the seminar. The focus will be on BBB and cerebral brain perfusion alterations, and the potential drug development for the longterm dysfunctions.
Invitant : Bordeaux Neurocampus / NBA
Responsable
- Nom : Julia GONCALVES