A5047648232- Alzheimer's disease research and treatments
- Protease and Inhibitor Mechanisms
- NF-κB Signaling Pathways
- Neuroinflammation and Neurodegeneration Mechanisms
- Nuclear Receptors and Signaling
- S100 Proteins and Annexins
- interferon and immune responses
- Psoriasis: Treatment and Pathogenesis
- Olfactory and Sensory Function Studies
- Cell Adhesion Molecules Research
- Cholinesterase and Neurodegenerative Diseases
- Stress Responses and Cortisol
- Protein Hydrolysis and Bioactive Peptides
- Vitamin D Research Studies
- Tryptophan and brain disorders
- Signaling Pathways in Disease
- GDF15 and Related Biomarkers
- Machine Learning in Bioinformatics
- Trace Elements in Health
- Chemokine receptors and signaling
- Biochemical Analysis and Sensing Techniques
- Blood Coagulation and Thrombosis Mechanisms
- Cancer Research and Treatment
- Spondyloarthritis Studies and Treatments
- RNA regulation and disease
Centre National de la Recherche Scientifique
2013-2024
Aix-Marseille Université
2013-2024
Institut de Neurophysiopathologie
2012-2024
Hôpitaux Universitaires de Strasbourg
2019
École Pratique des Hautes Études
2012-2019
Université Gustave Eiffel
2017
Previously, we demonstrated i) that ergocalciferol (vitamin D2) increases axon diameter and potentiates nerve regeneration in a rat model of transected peripheral ii) cholecalciferol D3) improves breathing hyper-reflexia paraplegia. However, before bringing this molecule to the clinic, it was prime importance assess which form - versus dose were most efficient identify molecular pathways activated by pleiotropic molecule. The left peroneal cut out on length 10 mm autografted an inverted...
Apolipoprotein E4 (APOEε4) is the major allelic risk factor for late-onset sporadic Alzheimer's disease (sAD). Inflammation increasingly considered as critical in sAD initiation and progression. Identifying brain molecular mechanisms that could bridge these two factors remain unelucidated. Leveraging induced pluripotent stem cell (iPSC)-based strategies, we demonstrate APOE controls inflammation human astrocytes by regulating Transgelin 3 (TAGLN3) expression and, ultimately, nuclear κB...
The TNF ligand family member TWEAK exists as membrane and soluble forms is involved in the regulation of various human inflammatory pathologies, through binding to its main receptor, Fn14. We have shown that form has a pro-neuroinflammatory effect an animal model multiple sclerosis we further demonstrated blocking activity during recruitment phase immune cells across blood brain barrier (BBB) was protective this model. It now well established endothelial periphery astrocytes central nervous...
We previously reported that deficiency of membrane-type five matrix metalloproteinase (MT5-MMP) prevents amyloid pathology in the cortex and hippocampus 5xFAD mice, ameliorates functional outcome. have now investigated whether integrity another important area affected Alzheimer's disease (AD), frontal cortex, was also preserved upon MT5-MMP 4-month old mice at prodromal stages pathology. used olfactory H-maze (OHM) to show learning impairment associated with dysfunctions prevented bigenic...
With an onset under the age of 3 years, autism spectrum disorders (ASDs) are now understood as diseases arising from pre- and/or early postnatal brain developmental anomalies insults. To unveil molecular mechanisms taking place during misshaping developing brain, we chose to study cells that representative very stages ontogenesis, namely stem cells. Here report on MOlybdenum COfactor Sulfurase (MOCOS), enzyme involved in purine metabolism, a newly identified player ASD. We found adult nasal...
Membrane-type matrix metalloproteinase 5 (MT5-MMP) deficiency in the 5xFAD mouse model of Alzheimer's disease (AD) reduces brain neuroinflammation and amyloidosis, prevents deficits synaptic activity cognition prodromal stages disease. In addition, MT5-MMP interleukin-1 beta (IL-1β)-mediated inflammation peripheral nervous system. this context, we hypothesized that MT5-MMP/IL-1β tandem could regulate nascent AD pathogenic events developing neural cells shortly after onset transgene...
We previously demonstrated that membrane type 1 (MT1) matrix metalloproteinase (MMP) was up-regulated in the hippocampus of model transgenic mice bearing 5 familial mutations on human amyloid precursor protein (APP) and presenilin Alzheimer disease (AD), proteinase increased levels β peptide (Aβ) its APP C-terminal fragment 99 aa a heterologous cell system. Here we provide further evidence MT1-MMP interacts with promotes amyloidogenesis proteolytic-dependent manner Swedish APP-expressing...
Stem cell-based therapies critically rely on selective cell migration toward pathological or injured areas. We previously demonstrated that human olfactory ectomesenchymal stem cells (OE-MSCs), derived from an adult lamina propria, migrate specifically mouse hippocampus after transplantation in the cerebrospinal fluid and promote functional recoveries. However, mechanisms controlling their recruitment homing remain elusive. Using vitro model of blood-brain barrier (BBB) secretome analysis,...
Inflammation and demyelination are the main processes in multiple sclerosis. Nevertheless, to date, blood biomarkers of inflammation lacking. TWEAK, a transmembrane protein that belongs TNF ligand family, has been previously identified as potential candidate. Twenty-eight patients (9 males, 19 females) were prospectively included after first clinical episode suggestive sclerosis clinically followed during 3 years. Fifty-seven healthy controls also included. TWEAK serum levels MRI exams...
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TNF weakly inducer of apoptosis (TWEAK) is member the ligand superfamily. Various data support that TWEAK produced by synovial macrophages may contribute to synovitis observed in psoriatic arthritis (PsoA). In PsoA, anti-TNF therapy has been successful agreement with key role pathogenesis and generation PsoA patients autoantibodies referred as "beneficial autoimmunity pro-inflammatory mediators". However, TNF-alpha regulation modulation inflammation during remains unknown.We have studied...
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member the TNF ligand family involved in various diseases including brain inflammatory pathologies such as multiple sclerosis. It has been demonstrated that TWEAK can induce cerebrovascular permeability an vitro model blood-brain barrier. The molecular mechanisms playing role versus TNFα signaling on cerebral microvascular endothelial cells are not well defined. Therefore, we aimed to identify gene expression changes cultures...
Abstract Background We previously reported that membrane-type 5-matrix metalloproteinase (MT5-MMP) deficiency not only reduces pathological hallmarks of Alzheimer’s disease (AD) in 5xFAD (Tg) mice vivo, but also impairs interleukin-1 beta (IL-1β)-mediated neuroinflammation and Ab production primary Tg immature neural cell cultures after 11 days vitro. now investigated the effect MT5-MMP on incipient pathogenic pathways are activated cortical at 21-24 vitro (DIV), during which neurons...
We previously reported that membrane-type 5-matrix metalloproteinase (MT5-MMP) deficiency not only reduces pathological hallmarks of Alzheimer's disease (AD) in 5xFAD (Tg) mice vivo but also impairs interleukin-1 beta (IL-1β)-mediated neuroinflammation and Aβ production primary Tg immature neural cell cultures after 11 days vitro. now investigate the effect MT5-MMP on incipient pathogenic pathways are activated cortical at 21-24 vitro (DIV), during which time neurons organized into a...
ABSTRACT The Apolipoprotein E4 ( APOE4 ) is the major allelic risk factor for late-onset Alzheimer’s disease (AD). associates with a pro-inflammatory phenotype increasingly considered as critical in AD initiation and progression. Yet, mechanisms driving an APOE4-dependent neuroinflammation remain unelucidated. Leveraging patient specific human induced Pluripotent Stem Cells (iPSCs) we demonstrate inflammatory chronicity hyperactivated responses upon cytokines astrocytes via novel mechanism....
<h3>Background</h3> TWEAK (TNF weakly inducer of apoptosis) is a type II-transmembrane protein, member the TNF ligand superfamily that can be cleaved to function as soluble cytokine. Depending on target cell and micro-environmental conditions, triggers multiple cellular responses ranging from modulation inflammation death. Various data support produced by synovial macrophages may contribute synovitis in human chronic inflammatory arthritis especially psoriatic (PsoA). In PsoA, anti-TNF...