A5076494986- Alzheimer's disease research and treatments
- Transplantation: Methods and Outcomes
- RNA regulation and disease
- Neuroinflammation and Neurodegeneration Mechanisms
- Renal Transplantation Outcomes and Treatments
- Cholinesterase and Neurodegenerative Diseases
- Inflammasome and immune disorders
- Cardiac Structural Anomalies and Repair
- MicroRNA in disease regulation
- Viral Infections and Immunology Research
- Cerebrovascular and genetic disorders
- Advanced Neuroimaging Techniques and Applications
- Organ Transplantation Techniques and Outcomes
- Advanced MRI Techniques and Applications
- 14-3-3 protein interactions
- Endoplasmic Reticulum Stress and Disease
- Neuroscience and Neuropharmacology Research
- Functional Brain Connectivity Studies
- Nuclear Receptors and Signaling
- Multiple Sclerosis Research Studies
- Heme Oxygenase-1 and Carbon Monoxide
- Phagocytosis and Immune Regulation
- Cardiac Fibrosis and Remodeling
- Advanced Glycation End Products research
- Complement system in diseases
Inserm
2015-2025
Neurocentre Magendie
2021-2025
Université de Bordeaux
2021-2025
Sorbonne Université
2014-2023
Institut du Cerveau
2023
Centre National de la Recherche Scientifique
2023
Assistance Publique – Hôpitaux de Paris
2011-2020
Sahlgrenska University Hospital
2020
University of Gothenburg
2020
Hôpital Fernand-Widal
2018
Rejection is one of the major causes late cardiac allograft failure and at present can only be diagnosed by invasive endomyocardial biopsies. We sought to determine whether microRNA profiling could serve as a non-invasive biomarker rejection.We included 113 heart transplant recipients from four referral French institutions (test cohort, n = 60, validation 53). In test we compared patients with acute biopsy-proven rejection (n 30) matched control without 30), assessing microRNAs expression in...
To assess the ability of a combination synaptic CSF biomarkers to separate Alzheimer disease (AD) and non-AD disorders help in differential diagnosis between neurocognitive diseases.This was retrospective cross-sectional monocentric study. All participants explored with assessments for decline were invited participate. After complete clinical imaging evaluations, 243 patients included. (GAP-43, neurogranin, SNAP-25 total, SNAP-25aa40, synaptotagmin-1) AD blindly quantified ELISA or mass...
Alzheimer's disease (AD) is a neurodegenerative disorder, marked by senile plaques composed of amyloid-β (Aβ) peptide, neurofibrillary tangles, neuronal loss and neuroinflammation. Previous works have suggested that systemic inflammation could contribute to neuroinflammation enhanced Aβ cerebral concentrations. The molecular pathways leading these events are not fully understood. PKR pro-apoptotic kinase can trigger accumulates in the brain cerebrospinal fluid AD patients. goal present study...
Memory impairment is one of the disabling manifestations multiple sclerosis (MS) possibly present from early stages disease and for which there no specific treatment. Hippocampal synaptic dysfunction dendritic loss, associated with microglial activation, can underlie memory deficits, yet molecular mechanisms driving such hippocampal neurodegeneration need to be elucidated. In early-stage experimental autoimmune encephalomyelitis (EAE) female mice, we assessed expression level molecules...
Abstract Ischemic strokes disrupt brain networks, leading to remote effects in key regions like the thalamus, a critical hub for functions. However, non-invasive methods quantify these consequences still need be explored. This study aimed demonstrate that MRI-derived R2* changes can capture iron accumulation linked with inflammation secondary stroke-induced disconnection. In order link disconnection, we first conducted analysis of 156 prospectively included stroke patients who underwent MRI...
Abstract Brain lesions in Alzheimer's disease (AD) include amyloid plaques made of Aβ peptides and neurofibrillary tangles composed hyperphosphorylated tau protein with synaptic neuronal loss neuroinflammation. oligomers can trigger phosphorylation alterations through activation kinases leading to progressive cognitive decline. PKR is a ubiquitous pro‐apoptotic serine/threonine kinase, levels activated are increased AD brains CSF. In addition, regulates negatively memory formation mice. To...
Abstract PKR is a cellular kinase involved in the regulation of integrative stress response (ISR) and pro-inflammatory pathways. Two N-terminal dsRNA Binding Domains (DRBD) are required for activation PKR, by interaction with either or PACT, another DRBD-containing protein. A role PACT inflammatory processes linked to neurodegenerative diseases has been proposed raised interest pharmacological inhibitors. However, inflammation subject controversy. We identified flavonoid luteolin as an...
Alzheimer's disease (AD) is characterized by accumulations of amyloid-β (Aβ42) and hyperphosphorylated tau proteins, associated with neuroinflammation, synaptic loss, neuronal death. Several studies indicate that c-Jun N-terminal kinase (JNK) implicated in the pathological features AD. We have investigated 5XFAD mice, therapeutic effects Brimapitide, a JNK-specific inhibitory peptide previously tested higher concentrations another AD model (TgCRND8). Three-month-old wild-type littermate mice...
Metabolic disorders including obesity and type 2 diabetes are known to be associated with chronic inflammation obvious risk factors for Alzheimer's disease. Recent evidences concerning suggest that the metabolic inflammasome ("metaflammasome") mediates inflammation. The double-stranded RNA-dependent protein kinase (PKR) is a central component of metaflammasome. In wild (WT) PKR-/- mice, blood glucose, insulin lipid levels brain expression phosphorylated components metaflammasome—PKR, JNK,...
ABSTRACT Age-dependent accumulation of the brain pigment neuromelanin has been implicated in pathogenesis Parkinson’s disease (PD). In humans, intracellular and extracellular levels are increased PD postmortem brains boosting production rodents compromises neuronal function viability triggers a PD-like phenotype. Focused ultrasound shown to reduce ultraviolet light-induced skin hyperpigmentation guinea pig remove β-amyloid plaques Alzheimer’s mouse models. Here we show that repeated...
Ischemic strokes disrupt brain networks, leading to remote effects in key regions like the thalamus, a critical hub for functions. However, non-invasive methods quantify these consequences still need be explored. This study aimed demonstrate that MRI-derived R2* changes can capture iron accumulation linked with inflammation secondary stroke-induced disconnection. In order link R2 * disconnection, we first conducted analysis of 156 prospectively included stroke patients who underwent MRI at...
The neuropathological lesions of Alzheimer's disease (AD) are characterized by amyloid plaques made extracellular peptides (Aβ1–42, Aβ1–40) and neurofibrillary tangles composed abnormally phosphorylated tau protein. cause these accumulations is unknown but according to the cascade hypothesis, Aβ1–42 could trigger a series neuronal events leading kinases activation neurodegeneration. roles in accumulation BACE 1 (β-secretase 1, an APP cleaving enzyme) activity have been little explored...
Alzheimer’s disease (AD) is the most common neurodegenerative disease. AD neuropathologically characterized by extra-neuronal accumulations of beta-amyloid (Aβ) forming senile plaques and intra-neuronal hyperphosphorylated tau proteins, leading to neuroinflammation, synaptic loss neuronal death. Several studies indicate that c-Jun N-terminal kinase (JNK) implicated in pathological features including neurodegeneration. We have investigated for first time 5XFAD mice, disease-modifying...
Background Histological assessment of endomyocardial biopsies (EMB) is the gold standard for diagnosis acute rejection in heart transplantation. However, conventional by histopathology, despite its clinical utility, faces serious limitations terms diagnostic accuracy rejection, raising need developing complementary approaches. MicroRNAs (miRNAs) are endogenous, single-stranded molecules that may repress target gene expression through degradation mRNA and/or inhibition protein expression. The...
Background Late cardiac allograft loss is mainly associated with vasculopathy (CAV). The pathogenesis of CAV remains unclear and complex involving immune non-immune factors. We hypothesized that ABMR could be operating in failing heart allografts represent a contributing factor accelerated vasculopathy. Methods In this retrospective multicenter study we included 40 removed during retransplantation for terminal graft failure. performed complete phenotyping studied the vascular tree. This...