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Conférence mensuelle - Jérôme BadautGliovascular unit dysfunctions precede neuronal alterations after pediatric brain injury

Abstract :

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.

 

 

Selected publications

Last publications

Aquaporins through the brain in health and disease: From water to gas movements.Friscourt F, Badaut J.J Neurosci Res. 2017 Sep 27. doi: 10.1002/jnr.24155. [Epub ahead of print] No abstract available.

 Early to Long-Term Alterations of CNS Barriers After Traumatic Brain Injury: Considerations for Drug Development.Rodriguez-Grande B, Ichkova A, Lemarchant S, Badaut J.AAPS J. 2017 Sep 13. doi: 10.1208/s12248-017-0123-3. [Epub ahead of print]

 New biomarker stars for traumatic brain injury.Ichkova A, Badaut J.J Cereb Blood Flow Metab. 2017 Oct;37(10):3276-3277. doi: 10.1177/0271678X17724683. Epub 2017 Aug 17. No abstract available.

 Increase of aquaporin 9 expression in astrocytes participates in astrogliosis.Hirt L, Price M, Mastour N, Brunet JF, Barrière G, Friscourt F, Badaut J.J Neurosci Res. 2017 Apr 17. doi: 10.1002/jnr.24061. [Epub ahead of print]

 

Jérôme Badaut, PhD, CNRS, Team: Brain Molecular Imaging. INCIA (Jerome.badaut @ u-bordeaux.fr)

PhD seminar series

La Fédération Bordeaux Neurocampus, en concertation avec l'Ecole Doctorale SVS, met en place une série de conférences destinée à l'ensemble des étudiants effectuant leur thèse dans les laboratoires de neurosciences de Bordeaux Neurocampus. Les doctorants Neuroscience in Bordeaux Association (NBA) sont chargés de l'organisation. 

Modalités : tous les premiers vendredi de chaque mois à 11h30 (durée : 1h), puis pizzas avec les étudiants et rencontres avec les personnes intéressées l'après-midi

If you are interested to share pizzas and a good moment with him (12h30 - 14h), please register on this Doodle) (maximum 15 people, first-come-first-served!)



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