BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Bordeaux Neurocampus - ECPv4.9.10//NONSGML v1.0//EN
CALSCALE:GREGORIAN
METHOD:PUBLISH
X-WR-CALNAME:Bordeaux Neurocampus
X-ORIGINAL-URL:https://www.bordeaux-neurocampus.fr/en/
X-WR-CALDESC:Events for Bordeaux Neurocampus
BEGIN:VTIMEZONE
TZID:Europe/Paris
BEGIN:DAYLIGHT
TZOFFSETFROM:+0100
TZOFFSETTO:+0200
TZNAME:CEST
DTSTART:20250330T010000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
TZNAME:CET
DTSTART:20251026T010000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20251006T140000
DTEND;TZID=Europe/Paris:20251006T140000
DTSTAMP:20260510T124612
CREATED:20250728T121025Z
LAST-MODIFIED:20251003T182358Z
UID:186790-1759759200-1759759200@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Flore Marchaland
DESCRIPTION:Venue: BBS \nDefense in french \n\nFlore Marchaland \nTeam : Brain Nutrient Sensing and Cognitive Trajectory from Development to Aging (NutriMind)\nNutriNeuro \nTitle\nMechanistic role of polyunsaturated fatty acids in brain development and cognitive trajectory \nAbstract\nN-3 and n-6 polyunsaturated fatty acids (PUFA) are essential for mammals\, as they cannot be synthesized de novo and must therefore be provided by the diet. Once consumed\, PUFA are incorporated into cellular membranes\, where they play a major structural role. Among PUFA\, docosahexaenoic acid (DHA\, n-3) and arachidonic acid (ARA\, n-6) are long-chain PUFA (LC-PUFA) that are particularly enriched in the brain. They are respectively derived from the metabolism of α-linolenic acid (ALA\, n-3) and linoleic acid (LA\, n-6)\, their precursors found in plant-derived foods. LC-PUFA can also be directly supplied by animal-derived foods\, primarily marine sources for n-3 and terrestrial sources for n-6. LC-PUFA accumulate in the brain during the perinatal period during which they are transferred from the mother to the infant first via the placenta and subsequently through breast milk. Thus\, the supply of LC-PUFA to the infant largely depends on maternal dietary PUFA intake. However\, since the late 20th century\, changes in dietary habits have led to an increase in n-6 PUFA consumption alongside a decrease in n-3 PUFA intake. Epidemiological and clinical studies have highlighted an inverse correlation between maternal n-3 PUFA dietary intake and children’s cognitive performance. Furthermore\, experimental studies in rodents have shown that perinatal n-3 PUFA deficiency impairs cognitive functions as well as neuronal morphology and function in male offspring. However\, the underlying mechanisms and potential sex-specific differences remain poorly understood. \nIn this context\, the primary objective of my PhD research was to investigate the cellular and molecular mechanisms underlying the behavioral and neurobiological effects induced by perinatal n-3 PUFA deficiency in both male and female offspring. Additionally\, I examined whether maintaining n-3 PUFA through an innovative genetic approach could prevent these alterations. \nThe results obtained indicate that perinatal n-3 PUFA deficiency affects\, in some cases in a sex-dependent manner\, 1) brain profiles of PUFA and their oxygenated derivatives (oxylipins) ; 2) the trajectory of physical and motor development ; 3) spatial memory ; and 4) long-term synaptic plasticity in the hippocampus. Genetic maintenance of PUFA in offspring exposed to this perinatal n-3 PUFA deficiency enables 1) the prevention of impairments in spatial memory and long-term synaptic plasticity in the hippocampus ; 2) an increase in mature synapse density\, particularly glutamatergic synapses\, within the hippocampus ; 3) the promotion of a transcriptional signature associated with synapse and neuronal network maturation ; and 4) the generation of a unique brain oxylipin profile differing by sex. In contrast\, genetic modulation of PUFA synthesis specifically in CaMKII neurons\, which are predominantly glutamatergic\, is not sufficient to prevent alterations in the PUFA profile of hippocampal synaptosomes or to rescue memory deficits induced by perinatal n-3 PUFA deficiency. Finally\, this work also shows that perinatal n-3 PUFA deficiency alters the transcriptomic signature of hippocampal microglia only from three weeks after birth\, with no significant effects observed earlier in development\, in a sex-dependent manner. \nOverall\, my PhD work has shed light on the mechanisms by which perinatal n-3 PUFA deficiency impairs brain development and cognition\, disrupting synaptic and neuronal network maturation in the hippocampus at both the cellular and molecular levels. \nKeywords : Development\, Behavior\, Nutrition\, Microglia\, Synapse \nPublication\nDi Miceli\, M.\, Rossitto\, M.\, Martinat\, M.\, Marchaland\, F.\, Kharbouche\, S.\, Graland\, M.\, … & Layé\, S. (2024). Modified neuroimmune processes and emotional behaviour in weaned and late adolescent male and female mice born via caesarean section. Scientific Reports\, 14(1)\, 29807. \nJury\n\n\n\nDr Sophie LAYÉ\, Directrice de recherche INRAE\, Université de Bordeaux\, France\nDirectrice de thèse\n\n\nDr Pascale CHAVIS\, Directrice de recherche INSERM\, Université Aix-Marseille\, FrancePr Pierre GRESSENS\, Professeur\, Université Paris Diderot\, France \nDr Daniela COTA\, Directrice de recherche INSERM\, Université de Bordeaux\, France\nRapportriceRapporteur \nExaminatrice\n\n\nDr Émilie PACARY\, Chargée de recherche INSERM\, Université de Bordeaux\, France\nExaminatrice\n\n\nPr Christoph RUMMEL\, Professeur\, Université Justus Liebig de Giessen\, AllemagnePr Richard BAZINET\, Professeur\, Université de Toronto\, Canada \nDr Jean-Christophe DELPECH\, Chargé de recherche INRAE\, Université de Bordeaux\, France\nExaminateurInvité \nInvité\n\n\n\n  \n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-flore-marchaland/
CATEGORIES:Thesis
END:VEVENT
END:VCALENDAR