A5011251704- Alzheimer's disease research and treatments
- Mitochondrial Function and Pathology
- Autophagy in Disease and Therapy
- Toxoplasma gondii Research Studies
- RNA Research and Splicing
- Herpesvirus Infections and Treatments
- Prion Diseases and Protein Misfolding
- Extracellular vesicles in disease
- Bioinformatics and Genomic Networks
- Signaling Pathways in Disease
- Cytomegalovirus and herpesvirus research
- Genetics and Neurodevelopmental Disorders
- Cellular transport and secretion
- Neuroscience and Neural Engineering
- Cholinesterase and Neurodegenerative Diseases
- Retinal Imaging and Analysis
- Biochemical Acid Research Studies
- Biochemical and Molecular Research
- Computational Drug Discovery Methods
- 3D Printing in Biomedical Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Medicinal Plants and Bioactive Compounds
- Ferroptosis and cancer prognosis
- Machine Learning in Bioinformatics
- Retinal Diseases and Treatments
Université Côte d'Azur
2020-2025
Inserm
2016-2025
Institut de Biologie Moléculaire et Cellulaire
2025
Institut de Pharmacologie Moléculaire et Cellulaire
2020-2024
Centre National de la Recherche Scientifique
2020-2024
Canadian Nautical Research Society
2024
Université de Lille
2016-2023
Institut Pasteur de Lille
2016-2023
Centre Hospitalier Universitaire de Lille
2019-2023
Institut de Biologie Valrose
2023
Abstract Several lines of recent evidence indicate that the amyloid precursor protein-derived C-terminal fragments (APP-CTFs) could correspond to an etiological trigger Alzheimer’s disease (AD) pathology. Altered mitochondrial homeostasis is considered early event in AD development. However, specific contribution APP-CTFs structure, function, and mitophagy defects remains be established. Here, we demonstrate neuroblastoma SH-SY5Y cells expressing either APP Swedish mutations, or...
Genome-wide association studies (GWASs) have identified 19 susceptibility loci for Alzheimer's disease (AD). However, understanding how these genes are involved in the pathophysiology of AD is one main challenges "post-GWAS" era. At least 123 located within loci; hence, a conventional approach (studying by one) would not be time- and cost-effective. We therefore developed genome-wide, high-content siRNA screening used it to assess functional impact gene under-expression on APP metabolism....
Abstract Mitochondria dysfunctions and mitophagy failure have been associated with several Alzheimer’s disease (AD) related molecular actors including amyloid beta (Aβ) recently the precursor protein-C terminal fragments (APP-CTFs). The efficacy of process in neurons relies on regulated mitochondrial transport along axons involving a complex machinery. contribution protein (APP) its derived to machinery alterations AD not investigated before. We report herein change expression proteins (SNPH...
Abstract Although APP metabolism is being intensively investigated, a large fraction of its modulators yet to be characterized. In this context, we combined two genome-wide high-content screenings assess the functional impact miRNAs and genes on signaling pathways involved. This approach highlighted involvement FERMT2 (or Kindlin-2), genetic risk factor Alzheimer’s disease (AD), as potential key modulator axon guidance, neuronal process that depends regulation metabolism. We found directly...
Abstract Mitochondrial dysfunctions are key features of Alzheimer’s disease (AD). The occurrence these disturbances in the peripheral cells AD patients and their potential correlation with progression underinvestigated. We studied mitochondrial structure, function mitophagy fibroblasts from healthy volunteers at prodromal (AD-MCI) or demented (AD-D) stages. carried out studies clinical cognitive scores, namely, (i) Mini-Mental State Examination (MMSE) (ii) Dementia Rating-Scale Sum Boxes...
Morphological alterations of the endosomal compartment have been widely described in post-mortem brains from Alzheimer's disease (AD) patients and subjects with Down syndrome (DS) who are at high risk for AD. Immunostaining antibodies against markers such as Early Endosome Antigen 1 (EEA1) revealed increased size EEA1-positive puncta. In DS, peripheral cells blood mononuclear (PBMCs) fibroblasts, share similar phenotype even absence We previously found that PBMCs AD larger puncta,...
ABSTRACT In addition to small extracellular vesicles known as exosomes, cells release large containing mitochondria (EVMs). However, the molecular and functional characteristics of EVMs, well impact EVM secretion on spreading mitochondrial dysfunction between cells, remain unknown in context Alzheimer’s Disease (AD). Here, we provide an ultrastructural, biochemical, characterization EVMs isolated from expressing amyloid precursor protein (APP) with familial Swedish mutation (APPswe). We...
<title>Abstract</title> In addition to small extracellular vesicles known as exosomes, cells release large containing mitochondria (EVMs). The molecular and functional characteristics of EVMs, well the impact EVMs on spreading mitochondrial dysfunction between cells, remain unknown in context Alzheimer’s Disease (AD). Here, we provide an ultrastructural, biochemical, characterization isolated from neuroblastoma expressing amyloid precursor protein with familial Swedish mutations (APPswe). We...
Toxoplasma gondii is a eukaryotic parasite that forms latent cysts in the brain of immunocompetent individuals. The infection immune-privileged central nervous system linked to most complications. With no drug currently available eliminate infected hosts, consequences neurons' long-term are unknown. It has long been known T. specifically differentiates into form (bradyzoite) neurons, but how neuron responds remains be elucidated. We have established new vitro model resulting production...
Abstract Recent meta-analyses of genome-wide association studies identified a number genetic risk factors Alzheimer’s disease; however, little is known about the mechanisms by which they contribute to pathological process. As synapse loss observed at earliest stage disease, deciphering impact genes on formation and maintenance great interest. In this article, we report microfluidic co-culture device that physically isolates synapses from pre- postsynaptic neurons chronically exposes them...
Background: Mitochondrial structure and function alterations are key pathological features in Alzheimer disease (AD) brains. The adenosine monophosphate-activated protein kinase (AMPK) its downstream effector Unc-51 like autophagy activating 1 (ULK1) represent a node controlling mitochondria health, the alteration of which likely contribute to AD development. Methods: We designed this study investigate AMPK-ULK1 activation state post-mortem human sporadic brains, 3xTgAD mice that...
<title>Abstract</title> Mitochondria dysfunctions and mitophagy failure have been associated with several Alzheimer’s disease (AD) related molecular actors including amyloid beta (Aβ) recently the precursor protein-C terminal fragments (APP-CTFs). The efficacy of process in neurons relies on regulated mitochondrial transport along axons involving a complex machinery. contribution protein (APP) its derived to machinery alterations AD not investigated before. We report herein change expression...
Abstract Recent meta-analyses of genome-wide association studies identified a number genetic risk factors Alzheimer’s disease; however, little is known about the mechanisms by which they contribute to pathological process. As synapse loss observed at earliest stage disease, deciphering impact genes on formation and maintenance great interest. In this paper, we report microfluidic co-culture device that physically isolates synapses from pre- postsynaptic neurons chronically exposes them toxic...
ABSTRACT Although APP metabolism is being intensively investigated, a large fraction of its modulators are yet to be characterized. In this context, we combined two genome-wide high-content screenings assess the functional impact miRNAs and genes on signaling pathways involved. This approach highlighted involvement FERMT2 (or Kindlin-2), genetic risk factor Alzheimer’s disease (AD), as potential key modulator axon guidance; neuronal process that depends regulation metabolism. We found...
ABSTRACT INTRODUCTION Mitochondria dysfunctions are key features in Alzheimer’s disease (AD). The occurrence of these disturbances AD patient’s peripheral cells and their potential correlation with progression under investigated. METHODS We studied mitochondrial structure, function mitophagy fibroblasts including healthy volunteers patients at the prodromal (AD-MCI) or demented (AD-D) stages. carried out studies clinical cognitive scores, Aβ plaques burden accumulation amyloid precursor...
Abstract Background FERMT2 has been identified as a genetic risk factor for AD. We have reported that the protein is partner of APP and loss (kindlin‐2) function altered both axonal growth long‐term potentiation in an APP‐dependent manner. In this study, we aimed to identify molecular mechanisms leading function. Method proteases other factors regulate cleavage protein, which appears be mechanism modulates its functions. The impact on interactions were analyzed by Co‐IP WB. Consequences...
Abstract Background Thanks to Genome‐Wide Association Studies (GWAS), 75 susceptibility loci for Alzheimer’s disease (AD) have been identified (Bellenguez et al, Nat genetics. 2022). However, one of the greatest challenges resides in understanding functional consequences these genetic determinants. One main hypothesis would be that some factors could involved APP metabolism and Aβ production. Indeed, even if numerous players characterized over last 20 years, a large part is still unknown....
Abstract Background Although APP metabolism is being intensively investigated, a large fraction of its modulators are yet to be characterized. In this context, we combined two genome‐wide high‐content screenings assess the functional impact miRNAs and genes on signaling pathways involved. Method We identify (n = 2,555) target 18,107) involved in metabolism. To predict function(s) that these genes, pathway enrichment analysis was performed using DIANA Tools mirPath (v3.0). CRISPR/Cas9...