Institut de Neurosciences Cognitives et Intégratives d'Aquitaine (UMR5287)

Aquitaine Institute for Cognitive and Integrative Neuroscience

Université de Bordeaux

Zone nord Bat 2 2ème étage
146, rue Léo Saignat
33076 Bordeaux cedex


Supervisory authorities

CNRS Ecole Pratique des Hautes Etudes Université de Bordeaux

Our partners

Neurocampus Unitéde Formation de Biologie


GDR Robotique GDR Mémoire GDR Multi-électrodes


Home > Directory

Badaut Jerome

by Joel Swendsen - published on , updated on

Jérôme Badaut, PhD

+33 (0)5 57 57 17 35

Site : Carreire


Brain Molecular Imaging


Neurovascular unit physiology/ traumatic brain injury/ stroke/ edema/ astrocytes

Research axis:

  • Neurovascular unit dysfunctions at longterm after juvenile traumatic brain injury
  • Role of the astrocyte network in Edema process

Scientific expertise:

  • In vivo models of traumatic brain injury
  • Immunohistochemistry and image analysis
  • RNAi in vivo
  • Astrocyte and organotypic cultures

The neurovascular unit (NVU) is composed of cerebral blood vessels, neurons, and scattered in between them, an astrocyte sheath. The homeostasis of this unit is critical for normal brain function and activity, especially the maintenance of blood-brain barrier (BBB) properties that regulate entry of blood components and clearance of brain waste. The astrocyte network contributes to water and ion homeostasis, as well as brain energy metabolism.
Our research is focused on the changing physiological properties of the NVU after traumatic brain injury (TBI). TBI can occur at any point in a person’s lifetime, affects a large number of soldiers in the battlefield, and is known to result in both short- and long-term consequences. The functional and molecular consequences after TBI might be a result of the changing NVU properties observed near the TBI injury site, and at a distance from the site of the impact. We are currently investigating the molecular mechanisms behind TBI-induced dysfunctions in NVU homeostasis using a rodent model. We evaluate these changes using magnetic resonance imaging (MRI), behavioral testing paradigms, and histological and molecular biology techniques to address specific protein targets at the NVU interface (for example: aquaporins…). We hope our understanding of these basic mechanisms will help to generate new target-specific drugs to promote functional recovery of individuals affected by brain injury.


  • ERA-NET NEURON, CnsAflame
  • R01 HD061946, NIH/NICHD
  • Fondation des Gueules cassees

Selected Publications:

1) A.M. FUKUDA, A. ADAMI, V. POP, J.A. BELLONE, J.S. COATS, R.E. HARTMAN, S. ASHWAL, A. OBENAUS, J. BADAUT. Posttraumatic reduction of edema with aquaporin-4 RNA interference improves acute and chronic functional recovery. J of Cereb Blood flow and Metab 2013 Oct;33(10):1621-32

2) V. POP, D.W. SORENSEN, J.E. KAMPER, D. O. AJAO, M. P. MURPHY, E. HEAD, R.E. HARTMAN, J. BADAUT (2013) Early brain injury alters the blood-brain barrier phenotype in parallel with beta-amyloid and cognitive changes in adulthood. J Cereb Blood Flow Metab Feb;33(2):205-14.

3) J. ZHANG, J.BADAUT, R. E. HARTMAN, A. OBENAUS, J. TANG, W.J. PEARCE. The Vascular Neural Network: Old Wine in a New Bottle? Nature Neurology Review. 2012 Nov 13;8(12):711-6

4) D.O. AJAO, V. POP, J. E. KAMPER, A. ADAMI, E. RUDOBECK, L. HUANG, R. VLKOLINSKY, R. E. HARTMAN, S. ASHWAL, A. OBENAUS, J. BADAUT Traumatic brain injury in young rats leads to progressive behavioral deficits coincident with altered myelin in adulthood. J. Neurotrauma, (Jul);29(11):2060-74

5) J.E. KAMPER, V. POP V, A.M. FUKUDA, D.O. AJAO, R.E. HARTMAN, J. BADAUT. Juvenile traumatic brain injury evolves into a chronic brain disorder: Behavioral and histological changes over 6 months. Exp Neurol. 2013 Sep 25;250C: 8-19