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

Aquitaine Institute for Cognitive and Integrative Neuroscience



INCIA - UMR 5287- CNRS
Université de Bordeaux

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

Téléphone 05.57.57.15.51
Télécopie 05.56.90.14.21

Supervisory authorities

CNRS Ecole Pratique des Hautes Etudes Université de Bordeaux

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Neurocampus Unitéde Formation de Biologie

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The next INCIA monthly seminar : Wednesday, November 13, from 11h30 am to 12h30 pm in the meeting room of building 2A (second floor) in Carreire.

by Loïc Grattier - published on

The speakers will be:

Maurice Garret (Neurobiology of Behavior):

Does the mutation of the huntingtin protein, linked to Huntington disease, alter the development?

Huntington disease is a neurodegenerative disease associated with the mutation of the Huntington protein, whose expression begins during the embryonic stage but is required at all developmental stages. The role of the mutation of the protein in the neurodegenerative process of the disease is well documented, but its contribution to an alteration of the development still remains to be established. Our behavioral, electrophysiology and molecular works show that brain functions are altered before the start of the disease’s symptoms, supporting the idea that neurodevelopmental alterations occur in subjects carrying the mutation. Our preliminary data show that the spatial distribution of FoxP2-expressing neurons is modified in a mouse model of the disease as early as the first post-natal days. Given the role of FoxP2 in brain development and motor functions, our data support the view of an altered brain development. Because a normal brain development requires a timely accurate migration of neurons, our observation is an opportunity to study the developmental aspect of the Huntington Disease.

Wei Yuan (invited researcher, The First Hospital of China Medical University, Shenyang - CPGs Team) :

Autophagy induction contributes to the neuroprotective effect of intermittent fasting in experimental spinal cord injury.Spinal cord injury (SCI) is one of the leading causes of neurological disability and death. So far, there is no satisfactory treatment for spinal cord injury due to its complex and ill-defined pathophysiology. Recently, autophagy has been implicated to be protective in acute spinal cord injury rat models. In this study, we aimed to investigate the therapeutic value of a dietary intervention, namely, intermittent fasting (IF), on neuronal survival after acute SCI and its underlying mechanism relating to autophagy regulation.