A5102019445- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- RNA regulation and disease
- Neuroscience and Neuropharmacology Research
- Neurotransmitter Receptor Influence on Behavior
- RNA Research and Splicing
- Autophagy in Disease and Therapy
- Parkinson's Disease Mechanisms and Treatments
- Tryptophan and brain disorders
- Endoplasmic Reticulum Stress and Disease
- Nuclear Receptors and Signaling
- Receptor Mechanisms and Signaling
- interferon and immune responses
- S100 Proteins and Annexins
- Neurological disorders and treatments
- RNA Interference and Gene Delivery
- Nicotinic Acetylcholine Receptors Study
- Neurogenesis and neuroplasticity mechanisms
- Mitochondrial Function and Pathology
- MicroRNA in disease regulation
- Neurological Disease Mechanisms and Treatments
- Protein Kinase Regulation and GTPase Signaling
- Glycosylation and Glycoproteins Research
- Click Chemistry and Applications
- Vitamin C and Antioxidants Research
Université de Poitiers
2013-2024
AnaBios (United States)
2019
MRC Biostatistics Unit
2015
Washington University in St. Louis
2014
France Alzheimer et maladies apparentées
2012-2014
Brain Physiology Lab
2011
Centre National de la Recherche Scientifique
2001-2010
UCLouvain
2000-2002
Centre Antoine Lacassagne
2001
University of Brescia
2001
Abstract In Alzheimer's disease, neuropathological hallmarks include the accumulation of β‐amyloid peptides (Aβ) in senile plaques, phosphorylated tau neurofibrillary tangles and neuronal death. Aβ is major aetiological agent according to amyloid cascade hypothesis. Translational control includes phosphorylation kinases mammalian target rapamycin (mTOR) p70S6k which modulate cell growth, proliferation autophagy. It mainly part an anti‐apoptotic cellular signalling. this study, we analysed...
One of the pathological hallmarks Alzheimer's disease (AD) is deposition extracellular amyloid-β (Aβ) peptide, which generated from cleavage amyloid precursor protein (APP). Accumulation Aβ thought to associate with progressive neuronal death observed in AD. However, precise signaling mechanisms underlying action AD pathophysiology are not completely understood. Here, we report involvement transcription factor signal transducer and activator 3 (STAT3) mediating Aβ-induced death. We find that...
Abstract Background Autophagy is a major pathway of protein and organelle degradation in the lysosome. exists at basal constitutive level can be induced as defense mechanism under stress conditions. Molecular relationships between autophagy inflammation periphery were recently evidenced, highlighting role regulation inflammation. Impairment (with accumulation autophagic vacuoles) substantial are found neurodegenerative diseases such Alzheimer’s Disease (AD). However, links AD remain to...
In recent years, studies have sought to understand the mechanisms involved in alteration of autophagic flux Alzheimer's disease (AD). Alongside description impairment lysosomal acidification, we wanted study relationships between inflammation and autophagy, two physiological components deregulated AD. Therefore, a longitudinal was performed APPswePS1dE9 transgenic mice at three, six twelve months age. Autophagic markers (Beclin-1, p62 LC3) activation mammalian Target Rapamycin (mTOR)...
Current evidence suggests a central role for autophagy in many neurodegenerative diseases including Alzheimer's disease, Huntington's Parkinson's disease and amyotrophic lateral sclerosis. Furthermore, it is well admitted that inflammation contributes to the progression of these diseases. Interestingly, crosstalks between have been reported vitro at peripheral level such as Crohn's disease. However, impact systemic on autophagic components brain remains be documented. Therefore, this study...
Inhibition of double‐stranded RNA‐dependent protein kinase (PKR) represents an interesting strategy for neuroprotection. However, inhibiting this which triggers the apoptotic process could favour in counterpart cell proliferation and tumorigenesis. Here, we use vivo model 7‐day‐old rat displaying a high activation brain PKR to investigate effects new inhibitor identified as oxindole/imidazole derivative (C16). We show first time that acute systemic injection C16 specifically inhibits...
There is considerable evidence that the activity of neuronal dopamine transporter (DAT) dynamically regulated and a putative implication its phosphorylation in this process has been proposed. However, there little information available regarding nature physiological stimuli contribute to endogenous control DAT function. Based on close relationship between glutamatergic dopaminergic systems striatum, we investigated modulation by metabotropic glutamate receptors (mGluRs). Short‐term...
Abstract Background Inflammation may be involved in the pathogenesis of Alzheimer's disease (AD). There has been little success with anti-inflammatory drugs AD, while promise treatment is more evident experimental models. A new strategy requires a better understanding molecular mechanisms. Among plethora signaling pathways activated by β-amyloid (Aβ) peptides, nuclear factor-kappa B (NF-κB) pathway could an interesting target. In virus-infected cells, double-stranded RNA-dependent protein...
Abstract Alzheimer's disease (AD) is a neurodegenerative of the central nervous system characterized by two major lesions: extracellular senile plaques and intraneuronal neurofibrillary tangles. β‐Amyloid (Aβ) known to play role in pathogenesis AD. Protein synthesis especially translation initiation are modulated different factors, including PKR/eIF2 mTOR/p70S6K pathways. mRNA altered brain AD patients. Very little about control mediated mTOR AD, although regulator also ribosome biogenesis...
For 10 years, research has focused on signaling pathways controlling translation to explain neuronal death in Alzheimer Disease (AD). Previous studies demonstrated different cellular and animal models AD patients that is down-regulated by the activation of double-stranded RNA-dependent protein kinase (PKR). Among downstream factors PKR, Fas-associated with a domain (FADD) subsequent activated caspase-8 are responsible for PKR-induced apoptosis recombinant virus-infected cells. However, no...