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X-WR-CALNAME:Bordeaux Neurocampus
X-ORIGINAL-URL:https://www.bordeaux-neurocampus.fr/en/
X-WR-CALDESC:Events for Bordeaux Neurocampus
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DTSTART:20260329T010000
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DTSTART;VALUE=DATE:20260929
DTEND;VALUE=DATE:20261016
DTSTAMP:20261006T132742
CREATED:20260303T224940Z
LAST-MODIFIED:20260923T223555Z
UID:196423-1790640000-1792108799@www.bordeaux-neurocampus.fr
SUMMARY:Cajal lectures - Neurovascular circuits
DESCRIPTION:Venue: CARF \n\nLectures are open to everyone \nThe Neurovascular Unit & Beyond – How CNS Border Sites Dynamically Regulate Brain Homeostasis\nTuesday\, September 29 \n9am – Robert Thorne (Denali University of Minnesota)\nIntroduction to the CNS barriers and related translational concepts. \nWednesday\, September 30 \n9am – Jerome Badaut (CNRS\, France)\nOut of the Cage: Wild Vertebrate Insights into CNS Borders and Neurovascular Biology. \nThursday\, October 1st \n9am – Nanna Macaulay (University of Copenhagen Denmark)\nChoroid plexus and CSF dynamics – the where\, which\, what\, and how of CSF secretion. \nSaturday\, October 3rd \n11am – Valentin Nagerl (Goettingen Germany)\nBarriers within: Imaging the extracellular space in the brain. \nMonday\, October 5 \n9am – Benoit Vanhollebeke (Université libre de Bruxelles Belgium)\nThe dynamic Blood-Brain Barrier: From Development to Modulation. \n11am – Jean-Francois Ghersi Egea (INSERM Lyon France)\nThe choroid plexus-CSF system in neurodevelopment and beyond: Relevance to CNS physiology\, pathology\, pharmaco-toxicology. \nTuesday\, October 6 (Venue: Centre Broca) \n9am – Brita Engelhardt (Theodor Kocher Institute University of Bern Switzerland)\nBrain barriers: the dynamic gatekeepers of CNS immune privilege and homeostasis. \n11am – Richard Daneman (University of California San Diego US)\nEvolution of the blood-brain barrier. \nThursday\, October 8 \n9am – Martin Lauritzen (University of Copenhagen Denmark)\nCerebral blood vessel physiology and the importance of the glycocalyx. \nMonday\, October 12 \n9am – Christer Betsholtz (Uppsala University / Karolinska Sweden)\nAn overview of the leptomeninges\, their physiology and their barrier properties. \n11am – Gou Young Koh (KAIST\, Korea Korea)\nMeningeal Lymphatics: A Novel Pathway for Brain Clearance. \nWednesday\, October 14 \n9am – Irena Loryan (Uppsala University Sweden)\nThe journey of small molecules to the brain: an introduction to neuro PK/PD Concepts and their applications. \n11am – Joy Zuchero (Denali Therapeutics\, US)\nUtilizing the Brain Vasculature for CNS Drug Delivery. \nThursday\, October 15 \n11am – Henrik Zetterberg (University of Gothenburg Sweden)\nUpdate on biofluid-based biomarkers for Alzheimer’s disease and other neurodegenerative dementias. \nFriday\, October 16 \n9am – Caroline Menard (University of Laval Canada)\nThe stressed blood-brain barrier: from resilience to depression. \n\n\nDetails about the course\nhttps://cajal-training.org/on-site/neurovascular-unit-beyond/ \n \n
URL:https://www.bordeaux-neurocampus.fr/en/event/cajal-lectures-neurovascular-circuits/
CATEGORIES:Cajal Lectures,For scientists,home-event
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DTSTART;TZID=Europe/Paris:20261006T140000
DTEND;TZID=Europe/Paris:20261006T140000
DTSTAMP:20261006T132742
CREATED:20260910T140604Z
LAST-MODIFIED:20260914T085406Z
UID:205919-1791295200-1791295200@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Clara-Fahia Toussaint
DESCRIPTION:Venue : BBS \n \nThesis defended in french \n\nIMN\nTeam: Physiopathology of proteinopathies \nThesis directed by Vincent Planche \nTitle\nIs Alzheimer’s disease unique to humans? \nAbstract\nAlzheimer’s disease (AD) is a major public health problem in our ageing Western societies. More than a century after it was first described\, there is still no consensus on the definition of AD. A purely biological view suggests that the mere presence of extracellular amyloid protein deposits and intracellular tau protein aggregates is sufficient to define the condition\, as these abnormalities are considered « causal» according to the amyloid cascade hypothesis. For other authors\, biological findings alone are insufficient for diagnosis and must be accompanied by clinical signs suggestive of progression towards dementia\, particularly as biological abnormalities may precede symptoms by 10 to 20 years\, and many healthy older people with amyloid deposits will never develop the disease. This nosological issue causes the estimated global prevalence to vary from 32 million (clinical-biological definition at the dementia stage) to 315 million people (biological definition)\, with major implications for future diagnostic and therapeutic strategies (plasma biomarkers\, anti-amyloid immunotherapies). \nThis issue is reflected in the representation of AD within the animal kingdom. Certain characteristic lesions have been reported in rodents\, cetaceans and elderly primates\, but these species do not develop all the characteristics of human tauopathy\, and the cognitive impact of these lesions remains uncertain. The very concept of dementia\, based on the loss of independence in everyday activities\, remains an anthropocentric definition with no equivalent in the animal kingdom. AD would therefore exist in animals according to a minimalist biological definition centred on amyloid\, but not according to a clinical-biological definition. \nThe first part of this thesis addresses this question through a systematic review of the literature on the presence of amyloid lesions and neurofibrillary tangles in non-human primates (38 articles\, 543 brains\, four species). Using logistic regression analyses\, this study shows that amyloid plaques follow an isometric pattern\, proportional to the lifespan of each species\, whilst neurofibrillary tangles (NFTs) follow a chronometric pattern\, appearing at a fixed time point (30 to 50 years) regardless of life expectancy. This dissociation challenges the hypothesis of the amyloid cascade as a universal mechanism and suggests that the full range of neuropathological lesions associated with AD is only present when a species’ lifespan allows these two independent processes to overlap. \nThe second part uses quantitative proteomics to compare the molecular signature of the human disease with that observed in macaques that have been injected with pathological tau proteins extracted from patients’ brains\, with or without co-injection of oligomeric Aβ. The human signature is not observed in macaques: there is no correlation between the two species\, as the model responds to the injection without replicating the molecular program of the human disease. \nThe third line of inquiry is based on the observation that longevity\, a necessary condition for the emergence of a clinically and biologically defined AD\, is not the sole factor influencing its manifestation at the population level. We developed an age-structured population model\, simulated on an individual-centred basis\, which combines demographic dynamics with the social allocation of care. This model shows that longevity alone is sufficient to cause the disease to emerge in a population\, and that healthcare does not trigger it but rather perpetuates it\, by prolonging the time lived with the disease. The evolutionary reconstruction further shows that the decline in adult mortality necessarily precedes the decline in the age at which people have children. \nKey words\nNon Human Primate\, Alzheimer\, care\, proteomic \nJury\nPresidente : Dr\, ABROUS Nora\nRapporteur : Dr\, POTIER Marie-Claude\nRapporteur : Pr\, KEUCK Lara\nExaminateur : MCF-PH\, VILLAIN Nicolas\nDirecteur de thèse : Pr\, LEMOINE Maël\nCo-Directeur : PU-PH\, PLANCHE Vincent\n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-clara-fahia-toussaint/
CATEGORIES:IMN,Thesis
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