18 march, 13h30 : Aurélie De Rus Jacquet, researcher at Laval University, at EBBS amphitheater
At the core of human existence lies a profound and intricate relationship with the plant world. Throughout our lives, we will rely on plants to breathe, eat, and heal, and Indigenous teachings across the globe recognize sacred properties to culturally symbolic medicinal plants. During this talk, we will explore the traditional and contemporary uses of herbal remedies to promote healthy aging and attenuate symptoms of neurodegenerative disorders. We will discuss conceptual and methodological approaches used in our laboratory to understand the biological mechanisms underlying the pro-health benefits of plant-based natural products. More specifically, our interest lies in the ability of these molecules to promote defense mechanisms in the aging brain by targeting non-neuronal brain cells, as these cell types regulate neuroinflammatory and neurotrophic processes involved in neuron survival. Experimental approaches to address these complex questions rely on cutting-edge technologies, such as induced pluripotent stem cells and the generation of 3D microfluidic and organoids-based modeling platforms. These exciting technologies – and others – hold promises to create more complex disease models that recapitulate the cytoarchitecture and dynamic cell-cell interactions characteristic of the human brain. Applying these tools to natural health product research in aging and neurodegenerative disorders has the potential to facilitate new discoveries and inform on their safety, efficacy and mechanisms of action.
Single cell rnaseq analysis of human cd34+ cells during their ex vivo expansion : Towards a better understanding and control of self-renewal process
30 octobre, 13h30-14h30 : Beatrice Passani (University of Florence)
The brain histaminergic system as a gateway for maladaptative stress-induced responses
22 June, 11h-12h: Lily Bentall (Department of Anatomy, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand), AMPHI BROCA
Changes in SNpr activity underlying dyskinesia in Parkinsonian model rats
Most (50-80%) Parkinson’s disease patients develop levodopa-induced dyskinesia (LID) within ten years of starting treatment. Once LID begins, limited treatments are available to reduce this side effect. We hypothesise irreversible changes occur within the cortico-basal ganglia-thalamo-cortical network as subsequent levodopa administration always produces dyskinesia.
We recorded GABAergic substantia nigra pars reticulata (SNpr) neuronal activity under urethane anaesthesia from dyskinetic (LID+), non-dyskinetic (LID-, lesioned rats dosed with levodopa but did not express LID), levodopa naïve PD-model (PD) and sham-lesioned (control, administered levodopa) rats. Firing rate, burstiness characteristics and LFP waveform features significantly changed between groups, related specifically to dyskinesia expression.
SNpr activity is altered by chronic levodopa administration. These changes hint that strengthened synaptic connections within the basal ganglia-thalamo-cortical network underlie dyskinesia expression. These findings could be important clinically to identify novel treatments that may reduce debilitating levodopa drug-induced side effects.
19 June, 13h30-14h30: Sophie Nicklaus (CSGA INRAE Dijon)
12 June, 13h30-14h30: Stéphanie Jougleux (Université de Bordeaux) : Présentation de la plateforme OSKAR
Résumé de la présentation :
Au cours de cette session, Stéphanie présentera la plateforme OSKAR Bordeaux, puis montrera comment y effectuer un dépôt en texte intégral avec export automatique vers HAL. Elle répondra également à vos questions sur l'open access. Contenu : - Présentation de l’interface de dépôt et des fonctionnalités d’OSKAR Bordeaux - Les étapes de publication et le processus de dépôt dans OSKAR / HAL
- Démonstration d'un dépôt dans OSKAR Bordeaux - L'interconnexion d'OSKAR et HAL, et l'export automatique d'un dépôt vers HAL - Les droits de diffusion des chercheurs (open access et Loi pour une République numérique, embargo...) - Temps d'échanges
Cette présentation sera en français.
5 June, 13h30-14h30: Heena Brown (Data scientist NutriMind team)
22 May, 13h30-14h30: Suzanne Van der Veldt (invité by par Pierre Trifilieff, at Broca)
15 may, 13h30-14h30 :
Sandrine Chantepie-Laborde, INRAE (15 min)
Zoé Masurie (Post-doc Food Circus team)
27 March, 13h30-14h30: Julie Chowen, Health Care System of the Community of Madrid
Dr. Julie Chowen is a Senior Investigator of the Health Care System of the Community of Madrid. She is Director of the Laboratory of Neuroendocrinology in the Department of Endocrinology at the Hospital Infantil Universitario Niño Jesús in Madrid since 2006. Dr. Chowen received her PhD in Physiology from the University of Washington in Seattle and then moved to Madrid to do a postdoctoral fellowship at the Instituto Cajal in Madrid. Her main areas of interest include neuroendocrinology, sexual dimorphism, obesity and metabolism. In recent years her investigation has concentrated on the role of glial cells in the physiology and pathophysiology of metabolism. She has published over
170 indexed articles in the area of neuroendocrinology and obesity.
27 February, 13h30-14h30: Serene Bondad, post-doc NutriNeuro in NutriMind team
30 January, 13h30-14h30 : Cédric Galera, médecin psychiatre de l’unité universitaire d’hospitalisation pour enfants et adolescents du CHU de bordeaux
16 December, 9h30-10h30: Mélanie Plourde, Neuroscience Sherbrooke, Canada : Est-ce que la mémoire dépend du lien sang-cerveau des oméga-3 ?
Chaire de recherche CRMUS sur le métabolisme des lipides lors du vieillissement, membre du RRI Food4BrainHealth
5 December, 13h30-14h30: Enrica Montalban: Involvement of the brain reward system in the regulation and dysregulation of feeding: from genetic vulnerability to the implication of astrocytes.
29 November, 13h-14h: second webinar of the AlimH/Giga institute (Belgium), Christina Schmidt from the In Vivo Imaging department of the Giga institute
Abstract :The presence of Alzheimer-disease (AD) brain biomarkers and subtle cognitive changes may be observed both in the preclinical stages of the disease and in healthy aging. However, few studies investigated if the association between biomarkers and cognition varies according to age. The COFITAGE cohort includes healthy participants from 50 to 70 y.o. followed during two years and phenotyped for cognition, affective state, allostatic load, lifestyle, sleep characteristics, amyloid / tau level deposits and brain atrophy. Preliminary analyses on 60 participants indicate that decline in executive performance on a 2 year period is associated to sleep efficiency in older participants only (over 60 y.o.). However, memory decline is not associated to hippocampal atrophy at baseline in any age group, while initial performance is related to hippocampal volumes in the older. These first results indicate age could influence the effect of some AD risk-factors on cognition.
7 November: Camille Amadieu: Gut microbiota, biological and psychological alterations in alcohol use disorder
24 October: Mounira Benasr: Macroscale and Microscale Depression-associated Architectural Alterations: Insights from Chronic Stress Models
Personal Statement: My work over the last 15 years has focused in studying the involvement of the structural changes associated with the pathophysiology and treatment of major depressive disorder (MDD). I believe that the improvement of our understanding of the cellular mechanisms implicated in the expression of the symptoms of depression will contribute to the development of new and more selective drugs for the treatment of this prevailing disorder. My lab use multidisciplinary approaches to investigate the effects of stress and antidepressant treatments on neuroplasticity in rodents. My lab focused on two consistent findings from human post-mortem studies in depression, the synaptic and astrocyte anomalies reported in MDD patients. Synaptic loss has been identified in human depression and consistently found in animals subjected to chronic stress models. Astrocytes are non-neuronal cells mainly involved in neurotrophic support of surrounding neurons and synaptic neurotransmission. Astroglial loss has been consistently reported in post-mortem brains from patients with depression and I demonstrated that astroglial loss is involved the development of depression-related behaviors. To identify the cellular mechanisms involved in the synaptic and astroglial losses associated with MDD, I primarily use rodent chronic stress models as chronic stress exposure induces behavioral deficits relevant to MDD pathology. To demonstrate the role of specific synaptic and astroglial changes associated with chronic stress in the development of depressive-like behaviors, my lab also employs transgenic, viral approaches to manipulate cells, genes and circuits. I believe that identifying the cellular mechanisms involved in both synaptic and astroglial dysfunctions associated with depression and chronic stress will help improve treatment of stress-related disorders. Therefore, using similar approaches, I also investigate if preventing or blocking chronic stress-induced synaptic and astroglial deficits reverse the behavioral and cellular effects of stress. Importantly, we also examine the relevance our findings using post-mortem brains from patients with MDD or translational approaches such as MRI. I strongly believe that this step of the research is essential to the validation and application of findings to clinical settings.
4 July: Lisa Roux
27 June: Ana Maria Cattaneo
13 June: Sophie Layé : Conférence ouverte à tout le département AlimH et l'institut GIGA de Liège
17 May 10h : Marie Labouesse, ETH Zurich (salle du conseil de l'UFR de Biologie)
Dissecting striato-pallidal circuit for motor control using in vivo optical approaches
16 May : Guillaume Dorothée, INSERM UMRS 938, Hôpital Saint Antoine
11 may 10h : Flavio Kapczinski, Université McMaster, Canada
The interplay of recurrent mood disorders and dementia
Salle du conseil de l'UFR de Biologie
11 april : Jean-Baptiste Penigault, Société Nanostring
Spatial transcritomic and proteomic solutions on slides
28 march: Maya Medalla
Prefrontal cortico-limbic networks in cognition: cellular and circuit diversity
Abstract: The goal my research is to develop an understanding of the synaptic and cellular diversity across distinct prefrontal pathways associated with high-order cognitive and emotional processes, and how this diversity relates to selective circuit vulnerability in disease in primates. To this effect I have employed multi-faceted anatomical and electrophysiological approaches at the systems, cellular and synaptic levels, combining whole-cell patch-clamp recording and intracellular labeling techniques in in vitro brain slices, with tract-tracing and multiple-immunolabeling techniques for confocal microscopy and 3D serial electron microscopy. The main question in my laboratory is to understand what differentiates excitatory, inhibitory and neuromodulatory circuits in the primate prefrontal cortex, and related sensory, motor and limbic cortices, that endow the capacity for complex high-order processing and underlie selective vulnerability in disease.
Title: Life without brain serotonin: Cognitive and social characterization of TPH2-ko rats in classical tests vs. automated home cage environment.
Abstract: Central serotonin is one major molecular target for treatment of several mental disorders. As such it appears a promising transdiagnostic biological marker of mental illness. A better understanding of the specific role of serotonin in the modulation of co-morbid impairments will be instrumental for the development of more efficient and personalized treatment for patients.
In this study, beyond a categorical view of mental disorders and in line with the search for endophenotypes, we aimed to expose the consequences of complete central serotonin deficiency on cognitive, social and everyday behaviors, using recently generated TPH2 knockout rats. We used a combination of state of the art semi-automated home-cage and stand-alone classical testing, a multidimensional profiling approach and unsupervised machine learning.
Although surprisingly, no cognitive function evaluated in classical tests were altered by the absence of brain serotonin, in the day-to-day context of the home-cage, the same TPH2-ko animals presented drastic changes in multiple aspects of their daily life with significant social disorganization (hierarchy and social networks). While developmental neurological compensations may have occurred these results challenge the concept of an essential role of serotonin for expressing cognitive abilities when tested in classical tests. Central serotonin appeared to be a key modulator of essential social and naturalistic home-cage behaviors when living in more complex environments. In the home-cage, TPH2-ko animals presented a profile reminiscent of the symptomatology of impulse control and anxiety disorders.
Our novel methodological framework to analyze an animal model under complex environmental conditions highlighted the importance to complement the use of classical behavioral tests with ethologically valid paradigms where the complexity of the animals’ natural behavior can be evaluated. This may in fact for some cases be the only way to discover subtle dysfunctions in animal models and which could effectively translate to human pathological conditions.
The general goal of my research is to map and dissect the neural circuits and to decipher the neuronal codes underlying the formation of internal representations of the external space within hippocampal-neocortical networks. In my talk, I will address two scientific directions. First,what are the neuronal ensemble mechanisms underlying the large capacity of the brain to rapidly encode and remember multiple sequential experiences? We recently uncovered the existence of internal generative predictive codes for the statistical regularities of the external space in the hippocampus that rely on the functional connectivity within and between high-repeat short motifs of sequential neurons called ‘tuplets’. This organization into neuronal tuplets segments extended temporal sequences into shorter modules, analogous to segmentation of words into syllables. This segmentation can vastly expand the generative encoding capacity of the network by rapidly combining neuronal tuplets into multiple independent extended sequences. Second, when and how do internally generated representations supporting memory formation and spatial/mental navigation emerge during brain development? I will discuss our work describing three distinct stages and timepoints in the postnatal development of time-compressed neuronal sequences of firing in the rat hippocampus area CA1 thought to be ethologically relevant for the emergence of memory encoding and consolidation.separation
Dr Tim Sargeant started his career in neuroscience with a PhD at Victoria University of Wellington, New Zealand. Tim went on to two postdoctoral positions at the Department of Medicine and the Department of Pathology at the University of Cambridge (UK) where he researched the cell’s recycling machinery (called the lysosomal system) and obtained training in molecular and cell biology. Tim was appointed to head of Lysosomal Health in Ageing in the Hopwood Centre for Neurobiology (formally the Lysosomal Diseases Research Unit) at SAHMRI in 2015. His current research focuses on the role of lysosomal recycling in common age-related disease such as Alzheimer’s disease. The lysosomal system is important for slowing cell ageing, as it removes damaged and unwanted material from the cell. This process is critically important for healthy brain function. Work from Lysosomal Health in Ageing has shown that this system is damaged in Alzheimer’s disease, and that changes in genes that are involved in the lysosomal system are associated with Alzheimer’s disease. Our current research focuses on development of methods for measurement of lysosomal system activity (through a process called autophagy) in humans. We are also developing interventions that improve the lysosomal system with the goal of delaying Alzheimer’s disease.
11 October: Aniko Korosi:
Aniko Korosi was a postdoc at UCI in the lab of dr. Baram (2006-2010) where she studied how enriched early life experience rewires the hypothalamus. At the end of 2010 she started her team and she is currently an Associate Professor at the University of Amsterdam. Her research is funded by several national and international programs (e.g. NWO Food Cognition and Behavior, NWO Meervoud, JPI- Nutri-Cog and ISAO). Her team includes several PhD students and postdocs and her research focuses on the programming of cognitive functions by early-life stress and aging and on the role of metabolic signals, nutrients and epigenetic mechanisms in this context. Her work encompasses pre-clinical work using an established mouse model of chronic early-life stress and clinical work and she is interested in developing peripheral (e.g. nutritional) intervention to prevent and/or reverse the lasting consequences of early-life stress as well as human studies investigating the effects of stress on breastmilk composition.
Early-life stress induced cognitive decline: a synergistic role for stress, nutrition and inflammation.
Abstract: Early-life stress (ES) is associated with increased vulnerability to cognitive impairments as well as metabolic disorders like obesity later in life. We investigate the role of a synergistic effect of stress, metabolic factors, nutrition and the neuroimmune system in this early-life induced programming.
We use an established model of chronic ES and expose mice to limited nesting and bedding material during first postnatal week and study the central and peripheral systems under basal and challenged conditions (i.e. LPS, amyloid accumulation, western style diet (WSD) and exercise) to gain further insight in the functionality of brain plasticity, neurogenesis microglia and adipose tissue. In addition, given the high nutritional demand during development, we propose that early nutrition is critical for programming of brain and body. We focus on essential micronutrients and fatty acids and propose that an early dietary intervention with a diet enriched with these nutrients might protect against ES-induced functional deficits.
We show that ES leads to cognitive impairments associated with reduced hippocampal neurogenesis at basal conditions as well as in response to exercise, primed microglia with exaggerated response to LPS or amyloid accumulation. Metabolically, ES mice exhibit a leaner phenotype but they accumulate more fat in response to WSD. Finally, with an early dietary intervention with micronutrient or fatty acid we were able to (at least partly) prevent ES-induced cognitive decline, likely mediated by modulation of microglia, without however affecting the ES-induced metabolic profile. These studies give new insights for the development of targeted dietary interventions for vulnerable populations.
Andrea Rau is a research scientist and biostatistician with strong expertise in omics data analysis and methods development. She currently holds a joint appointment at INRAE in the Animal Genetics and Integrative Biology (GABI) research unit and the BioEcoAgro joint cross-border research unit. Her research centers on “useable and useful” methodological developments for high-dimensional single- and multi-omics data analyses, including differential expression analyses, co-expression analyses, network inference, and integrative multi-omic analyses. As a strong proponent for the implementation and dissemination of methods in open-source software packages, she is an active user and developer of the R programming language, and has developed or co-developed several R packages and Shiny web applications. Over the past decade, she has successfully worked in close collaboration with biologists in animal, plant, and human genomics on interdisciplinary problems at the interface of statistics and biology.
Leveraging multi-comic data for integrative exploratory, predictive, and network analyses
Abstract: The increased availability and affordability of high-throughput sequencing technologies in recent years have facilitated the use of multi-omic studies, expanding and enriching our understanding of complex systems across hierarchical biological levels. Integrative methods for these heterogeneous and multi-faceted omics data have shown promise for enhancing the interpretability of exploratory analyses, improving predictive power, and contributing to a holistic understanding of systems biology. However, such integrative analyses are accompanied by several major obstacles, including the potentially ambiguous relationships among omic levels, high dimensionality coupled with small sample sizes, technical artefacts due to batch effects, potentially incomplete or missing data… and the occasional difficulty in posing well-defined and answerable research questions of such data. In light of these challenges, in this talk I will discuss a few of our recent methodological contributions to integrate multi-omic data for (1) exploratory analyses, (2) genomic prediction, and (3) network inference, all with a focus on enhanced interpretability and user-friendly software implementations.
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