A5007181072- Alzheimer's disease research and treatments
- Neuropeptides and Animal Physiology
- Peptidase Inhibition and Analysis
- Laser Applications in Dentistry and Medicine
- Cellular transport and secretion
- Cholinesterase and Neurodegenerative Diseases
- Connexins and lens biology
- Biochemical and Structural Characterization
- Migraine and Headache Studies
- Immune Response and Inflammation
- Diet and metabolism studies
- Neuroscience of respiration and sleep
- Dementia and Cognitive Impairment Research
- Retinoids in leukemia and cellular processes
- Photoreceptor and optogenetics research
- Extracellular vesicles in disease
- Neurobiology and Insect Physiology Research
- Endoplasmic Reticulum Stress and Disease
- Signaling Pathways in Disease
- Neuroinflammation and Neurodegeneration Mechanisms
- Computational Drug Discovery Methods
- Metabolism, Diabetes, and Cancer
- Diabetes Treatment and Management
- Environmental Toxicology and Ecotoxicology
Clinatec
2022-2024
Centre National de la Recherche Scientifique
2021-2023
Institut de Pharmacologie Moléculaire et Cellulaire
2018-2023
CEA Grenoble
2022
Commissariat à l'Énergie Atomique et aux Énergies Alternatives
2022
Inserm
2016-2022
Université Grenoble Alpes
2022
CEA LETI
2022
Université Côte d'Azur
2021
Institut de Génomique Fonctionnelle
2020
The processing of the amyloid precursor protein (APP) is one key events contributing to Alzheimer's disease (AD) etiology. Canonical cleavages by β- and γ-secretases lead Aβ production which accumulate in plaques. Recently, matrix metalloprotease MT5-MMP, referred as η-secretase, has been identified a novel APP cleaving enzyme producing transmembrane fragment, ηCTF that undergoes subsequent α- β-secretases yielding Aηα Aηβ peptides, respectively. functions contributions its related fragments...
The amyloid cascade hypothesis, which proposes a prominent role for full-length β peptides in Alzheimer's disease, is currently being questioned. In addition to peptide, several N-terminally truncated fragments of peptide could well contribute disease setting and/or progression. Among them, pyroGlu3–amyloid appears be one the main components early anatomical lesions disease–affected brains. Little known about proteolytic activities that account N-terminal truncations β, but they appear as...
Abstract One of the main components senile plaques in Alzheimer’s disease (AD)-affected brain is Aβ peptide species harboring a pyroglutamate at position three pE3-Aβ. Several studies indicated that pE3-Aβ toxic, prone to aggregation and serves as seed aggregation. The cyclisation glutamate residue produced by glutaminyl cyclase, pharmacological genetic reductions which significantly alleviate AD-related anatomical lesions cognitive defects mice models. 3 requires prior removal N-terminal...
Despite the ever-increasing role of pesticides in modern agriculture, their deleterious effects are still underexplored. Here we examine effect A6, a pesticide derived from naturally-occurring α-terthienyl, and structurally related to endocrine disrupting anilinopyrimidines, on living zebrafish larvae. We show that both A6 an anilinopyrimidine, cyprodinyl, decrease larval survival affect central neurons at micromolar concentrations. Focusing superficial easily observable sensory system,...
The etiology of Alzheimer's disease is far from being completely understood. Genetic approaches have helped in this matter and greatly supported the view that β-amyloid precursor protein (βAPP) could be at center gravity pathology. Thus, mutations responsible for autosomal dominant aggressive forms (AD) are all harbored by either βAPP itself or its cleaving enzyme presenilins 1/2 referred to as γ-secretase. It was therefore convincing note fully independent gene products harboring AD-linked...
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...
Abstract The processing of the amyloid precursor protein (APP) is one key events contributing to Alzheimer’s disease (AD) etiology. Canonical cleavages by β- and γ-secretases lead Aβ production which accumulate in plaques. Recently, matrix metalloprotease MT5-MMP, referred as η-secretase, has been identified a novel APP cleaving enzyme producing transmembrane fragment, ηCTF that undergoes subsequent α- β-secretases yielding Aηα Aηβ peptides, respectively. functions contributions its related...