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Venue: Bordeaux School of Neuroscience

The normal aging process is associated with reduced performance on cognitive tasks that require one to quickly process or transform information to make a decision, including measures of speed of processing, executive cognitive function, working and relational memories. Structural and functional alterations in the brain correlate with these age-related cognitive changes, such as loss of synapses, and dysfunction of neuronal networks. It is crucial to develop new approaches that consider the whole neuroanatomical, endocrine, immunological, vascular and cellular changes impacting on cognition.

This 3-week course will cover the fundamentals of cognitive aging -including inter-individual differences, cognitive and brain reserve and risk factors- and highlight the newest functional imaging methods to study human brain function. The Faculty will share the state-of-the-art molecular, optical, computational, electrophysiological, behavioural and epidemiological approaches available for studying the aging brain in diverse model systems. The Students will learn the potential and limitations of these methods, through practical experience in a combination of lectures addressing aging in both humans and animal models and hands-on-projects. They will acquire sufficient practical experience to model, design and interpret experiments and brainstorm on novel technologies and hypotheses to explore the aging of the brain using more integrative and creative approaches.

Keynote speakers:
Hélène Amieva - University of Bordeaux
Adam Antebi - MPI for Biology of Ageing
Carol Barnes - University of Arizona
LucBuée-Centrede Recherche Jean-Pierre Aubert
Gwenaëlle Catheline - University of Bordeaux
Maria Llorens-Martin - Centro de Biologia
Molecular Severo Ochoa
Aline Marighetto - University of Bordeaux
Lars Nyberg - Umeå University
Laure Rondi-Reig - Sorbonne University
Yaakov Stern - Columbia University
Tony Wyss-Coray - Stanford University

Course director: Luísa Lopes
Co-directors: Cheryl Grady and Nora Abrous

Application deadline: 25 May 2020
Stipends are available

Fee : 3.500 € (includes tuition fee, accommodation and meals)

The CAJAL programme offers 4 stipends per course (waived registration fee, not including travel expenses). Please apply through the course online application form. In order to identify candidates in real need of a stipend, any grant applicant is encouraged to first request funds from their lab, institution or government.

Kindly note that if you benefited from a Cajal stipend in the past, you are no longer eligible to receive this kind of funding. However other types of funding (such as partial travel grants from sponsors) might be made available after the participants selection process, depending on the course.

For enquiries, please contact: info@cajal-training.org

Pièces jointes

L’article montre (chez la souris) que (1) l’amnésie pour le contexte traumatique est une cause du développement du trouble de stress post-traumatique (TSPT) et que (2) la réactivation du souvenir traumatique dans l’environnement traumatique lui-même normalise la mémoire traumatique, c’est-à-dire traite cette mémoire pathologique en la re-contextualisant. Les individus se remémorent le trauma en l’associant spécifiquement au contexte d’origine, en conséquence, ils n’expriment plus de peur inappropriée relative au trauma dans n’importe quel contexte (comme cela est observé dans le TSPT). La publication montre aussi que cette normalisation de la mémoire implique une activation de l’hippocampe.

Al Abed S., Ducourneau E.G., Bouarab C., Sellami A., Marighetto* A., and Desmedt* A.
Preventing and treating PTSD-like memory by trauma contextualization.
Nature Communications.
2020 Aug 24;11(1):4220.
doi: 10.1038/s41467-020-18002-w.

*co-last authorship

Une étude de l’équipe Desmedt en collaboration avec PV Piazza & Lundbeck Lab.

Cet article montre (en collaboration avec le laboratoire Lundbeck) qu’une molécule connue comme anti-psychotique, le brexpiprazole, traite la mémoire traumatique chez la souris: elle bloque l’hypermnésie émotionnelle du trauma tout en améliorant la mémoire du contexte traumatique (déficitaire chez les sujets TSPT*). La mémoire traumatique est donc normalisée ainsi que la plupart des altérations d’activité au sein du réseau hippocampo-amygdalien sous-jacent. De manière assez remarquable, le papier montre aussi que cette molécule est plus efficace que des molécules classiquement utilisées dans cette pathologie (Prazosin, Excitalopram, Diazepam). Ces données pré-cliniques indiquent que le brexpiprazole pourrait constituer un nouveau traitement pharmacologique du TSPT en normalisant la mémoire traumatique.

* Trouble de Stress Post-Traumatique

Ducourneau E.G., Guette C., Perrot D., Mondesir M., Mombereau C., Arnt J. Desmedt* A. and Piazza* P.V. Brexpiprazole blocks Posttraumatic stress disorder-like memory while promoting normal fear memory. Molecular Psychiatry. 2020 Aug 19.
*co-last authorship.
doi: 10.1038/s41380-020-0852-z
Premier auteur

Eva Ducourneau
Equipe Marighetto/Desmedt
(« Physiopathologie de la mémoire déclaratarive »)

Aline Desmedt
Equipe Marighetto/Desmedt
(« Physiopathologie de la mémoire déclarative »)

Le prochain congrès « Aging 2018 » se tiendra au domaine du Haut Carré à Talence du 26 au 28 septembre 2018. Il réunira les membres de la communauté neuroscientifique internationale autour d’un thème central : le vieillissement cognitif en absence de MA et l’existence de différences inter-individuelles dans l’atteinte mnésique au cours de l’âge.

Invitant : Bordeaux Neurocampus, Gwenaelle Catheline, Aline Marighetto, Nora Abrous
L’inscription est obligatoire pour toute personne participant ou assistant au Congrès. La soumission d’un abstract ne peut se faire qu’après inscription. Le colloque accueillera un maximum de 280 personnes. Les participants sont tenus d'être présents durant les 3 jours.

Beau succès pour le congrès Aging co-organisé par Nora Abrous, Aline Marighetto et Gwenaelle Catherine pour faire le point sur les dernières découvertes concernant le vieillissement cognitif.

14/09/2018 11h30
Marloes Henckens

Meeting room: Amphi du Centre Broca

Dr. Marloes Henckens from Department of Cognitive Neuroscience, Donders Institute for Brain (Netherlands)'s lab will give a presentation entitled 'The neural signature of trauma susceptibility'

Invitant : Aline Desmedt, PhD , Maitre de Conférence au Neurocentre Magendie, Team Marighetto 'Pathophysiology of declarative memory'

Posttraumatic stress disorder (PTSD) is a psychiatric disorder which can develop after exposure to a traumatic event. Flashbacks, spontaneous recollection and recurrent nightmares of the trauma are amongst the most devastating symptoms of PTSD, through which patients continuously relive their trauma. Interestingly, only a small fraction (8-10%) of all trauma-exposed individuals eventually develops PTSD, whereas the rest is resilient and remains healthy. But how is the vulnerable brain different from the resilient one and when do these differences arise? Understanding the mechanisms behind these inter-individual differences could contribute to new clinical intervention strategies.
The use of a mouse model for PTSD allows us to study the mechanisms underlying relative resilience or susceptibility to PTSD in a longitudinal fashion, under controlled settings, while allowing for more invasive brain measurements. In this model, mice are first exposed to a traumatic event (i.e., severe unpredictable foot shock), followed by a trigger (i.e., mild predictable foot shock) in a different context one day later. Following a week of recovery, eventual development of PTSD-like symptomatology is assessed using a battery of behavioural tests to identify mice resilient and vulnerable to the trauma. Combining this model with functional MRI obtained both before and after trauma exposure, allowed us to study the development of a potential imbalance in neural network function as a consequence of trauma in the PTSD-vulnerable vs resilient brain, as well as the potential presence of neural abnormalities prior to trauma exposure in these animals. To study brain responses to the trauma itself, we used the so-called targeted recombination in active populations (TRAP) mice, in which the injection of tamoxifen opens up a temporal window in which all neurons expressing certain immediate early genes (reflecting neuronal activity), are permanently fluorescently labelled. We injected these animals with tamoxifen just prior to trauma exposure, and again assessed PTSD-symptoms later on. By re-exposing them to the traumatic context just before sacrifice and analysing trauma retrieval-induced neuronal activity by immunohistochemistry, we were moreover able to analyse the storage of the trauma memory into long-term memory. This allowed us to assess whether aberrant storage of the trauma memory could explain the emotional hypermnesia and contextual hypomnesia of the trauma that seem to characterize PTSD patients.

Les travaux de Catherine Benneteau sur les phytoestrogènes réalisés dans l'équipe d'Aline Marighetto ont fait l'objet d'un reportage diffusé dans "le Doc du dimanche" sur France 5. Retrouvez le passage consacré aux travaux magendiens à partie de 14'30".

31/01/2018 10h00
Christopher STEVENS from Marighetto's lab will give a presentation entitled "A behavioral mouse model for studying the neuronal underpinnings of confirmation bias"

18/12/2017 14h30
Eva-Gunnel DUCOURNEAU from Marighetto's lab will defend her Ph.D. thesis entitled 'Rôle de la plasticité cellulaire au sein du circuit hippocampo-amygdalien dans la formation d'une mémoire de peur normale ou traumatique'

from Marighetto's lab will defend her Ph.D. thesis entitled 'Rôle de la plasticité cellulaire au sein du circuit hippocampo-amygdalien dans la formation d'une mémoire de peur normale ou traumatique'
Date de la soutenance: 18/12/2017 - 14h30
Lieu: Neurocentre Magendie Seminar room

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/formation-doctorale/these-2017/eva-gunnel-ducourneau.html