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DTSTART;TZID=Europe/Paris:20201217T143000
DTEND;TZID=Europe/Paris:20201217T163000
DTSTAMP:20260310T151910
CREATED:20201119T094805Z
LAST-MODIFIED:20201204T162412Z
UID:128142-1608215400-1608222600@www.bordeaux-neurocampus.fr
SUMMARY:Thsesis defense - Ania Goncalves
DESCRIPTION:Online. \nSend an email to Ania Goncalves to get the link \n\nTitle : Altered neuronal activity in the hippocampal CA3 region in an in vitro model of tauopathy\nAnia Goncalves\nAnia Goncalves\nTeam Mulle\nIINS \nThesis supervisor:  Sandrine Pouvreau\, Chargée de recherche\, CNRS \nDefense in english \nSummary\nAlzheimer’s disease (AD) is a neurodegenerative disorder characterized by brain depositions of amyloid plaques and tau tangles. The propagation of the tauopathy correlates strongly with the cognitive decline in patients\, highlighting the critical role of tau in AD. Yet\, the mechanisms linking tauopathy and impaired brain functions remain elusive. Different in vitro and in vivo animal models have been used to study the pathological features related to tauopathies\, such as synaptic dysfunction\, impaired neuronal activity and neuronal loss. Nevertheless\, it is still challenging to find a model that allows the evaluation of the tau toxicity in a complex neuronal circuit with proper spatio-temporal resolution. Hence\, in this work\, we developed a physiologically relevant ex vivo model of ADlinked tauopathy\, based on organotypic hippocampal slices\, for the investigation at a proper spatiotemporal resolution of progressive impairments in neuronal physiology. We took advantage of the seeding properties of misfolded tau to induce tau pathology in organotypic hippocampal slices\, considering that the hippocampus is particularly vulnerable in AD. The hippocampal organotypic slices model shows a progressive accumulation of hyperphosphorylated tau and the main features of the disease such as accumulation of other pathological forms of tau\,   neurodegeneration and selective cellular vulnerability. Our in vitro model recapitulates the development of the disease observed in old transgenic mice. Additionally\, our model displays altered neuronal activity at late stages of the disease\, along with the accumulation of hyperphosphorylated tau and\nneuronal loss in CA3. Remarkably\, the pathological pattern of neuronal activity\, including hyperactivity and hypersynchrony\, could be reproduced in WT slices by simultaneous inhibition of GABAA and GABAB transmission. Our data suggest that impairment of GABAergic signalling underlies the altered neuronal activity found in tau pathology. \nKeywords: tau protein\, Alzheimer’s Disease\, network activity \nJury\nPrésident : \nDr. Giovanni MARSICANO\, Directeur de Recherche\, INSERM \nRapporteurs \nDr. Alexis BEMELMANS\, Chargé de recherche\, CEA \nDr. David BLUM\, Directeur de Recherche\, INSERM \nExaminateurs \nDr. Ilse DEWACHTER\, Professeur\, University Hasselt \nDr. Olivier NICOLE\, Chargé de recherche\, CNRS \nInvité \nDr. Juan PITA-ALMENAR\, Senior Scientist\, Janssen Pharmaceutica \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thsesis-defense-ania-goncalves/
CATEGORIES:Thesis
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