candice chapouly Tenure track researcher, CRCN Inserm U1034

Course and current status

11/2019-today               Tenure track researcher (CRCN Inserm)

Inserm U1034, Biology of cardiovascular diseases, Pessac, France


01/2018-11/2019          Postdoctoral researcher in Biology/Health

Inserm U1034, Biology of cardiovascular diseases, Pessac, France


01/2014-12/2017           Postdoctoral researcher in Biology/Health

Corinne Goldsmith Dickinson Center for Multiple Sclerosis, department of neurology, Friedman Brain Institute, Mount Sinai Hospital, New York City, United States                   


09/2009-01/2014           PhD student in Biology/Health

Inserm U1034 unit, cardiovascular adaptation to ischemia, Bordeaux, France               

Scientific summary

Neuronal cell loss, defined as neurodegeneration, is the major cause underlying behavioral and psychological abnormalities, notably in Alzheimer’s disease and multiple sclerosis. One common feature of neurodegeneration is Blood Brain Barrier (BBB) permeability and over the last decade, the hypothesis that it precedes and drives neurodegeneration is more and more imposing itself. However, a substantial intercellular communication occurs between the BBB and the surrounding glia. More specifically, to enter the CNS, soluble factors and immune cells must initially traverse the BBB. Then, they circulate within the perivascular space (PVS), a region separated from the parenchyma by a network of astrocytes called the Glia Limitans. While it is now well established that BBB breakdown is noxious in neuropathology, the role of the Glia Limitans appears trickier. Indeed, astrocytes, described as reactive, are emerging as “Dr Jekyll and Mister Hyde” cells which produce, pro-inflammatory/pro-permeability factors but also neuro-protective factors.


Strikingly, recent work uncovered a new role for reactive astrocytes as a physical barrier taking over once the BBB is open during neuro-inflammation. Thus, there isn’t one, but two barriers, protecting the parenchyma: the endothelial BBB and the astrocytic Glia Limitans which form the gliovascular unit. 


Our project aims to impose the concept of a reciprocally regulated double barrier system within the CNS so that the BBB is no longer considered the sole line of defense of the parenchyma. It is a necessary step towards a better management of neuropathology. Indeed, the main approach which focuses on targeting BBB to limit or to facilitate access to the parenchyma has failed so far as it is more likely that playing on BBB status impact Glia Limitans barrier properties. To meet our goal, we plan to unravel the gliovascular double barrier functioning in various neurovascular disorders and to identify molecular actors driving the gliovascular unit status.

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