Academic literature on the topic 'Peptide neurotrophique'
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Journal articles on the topic "Peptide neurotrophique":
Gressens, P. "Le peptide vasoactif intestinal : un nouveau facteur neurotrophique." Archives de Pédiatrie 5, no. 6 (June 1998): 654–60. http://dx.doi.org/10.1016/s0929-693x(98)80174-7.
Dissertations / Theses on the topic "Peptide neurotrophique":
Petit-Dop, Florence. "Effets de deux neurotrophines, BDNF et NT3, et d'un nouveau peptide, le "Melanin concentrating hormone Gene Overprinted Polypeptide" (MGOP) sur le développement de neurones hypophysiotropes de Rat in vitro." Paris 11, 2001. http://www.theses.fr/2001PA11T031.
ANGLARD, PATRICK. "Mise en evidence de l'action neurotrophique de l'hormone adrenocorticotrope (acth) et etude de ses mecanismes." Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR13102.
Rangon, Claire-Marie. "Importance des facteurs neurotrophiques dans la protection cérébrale périnatale : exemples du VIP et du BDNF." Paris 5, 2005. http://www.theses.fr/2005PA05S023.
The neonatal brain is often exposed to insults. We have developped a mice model allowing studies of neonatal brain lesions. On postnatal day 5, pups are injected intracerebrally with ibotenate, (NMDA agonist) resulting in both cortical and white matter lesions. When co-injected with ibotenate, vasoactive intestinal peptide (VIP) protects white matter. VIP binds to an atypical VPAC2 receptor that stimulate Kinase C Protein and triggers Brain-Derived Neurotrophic Factor (BDNF) induction and excretion by astrocytes. BDNF binds to neuronal TrkB receptors coupled to the Mitogen-Activated Protein Kinases pathway which stimulates sprouting and axonal re-growth. Nevertheless, BDNF can be powerless to protect the immature brain : prenatal chronic ultra_mild stress does exacerbate neonatal brain lesions while increasing BDNF mRNA content in male pups. However, injection of allosteric modulators of AMPA receptors (called AMPAkines) increases BDNF synthesis and decreases neonatal brain lesions
Wu, Yu. "Neuroprotective liquid crystalline cubosome and hexosome nanoparticle formulations by self-assembly of plasmalogen lipids and a neurotrophic peptide." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASQ003.
The primary aim of this thesis is to investigate the neuroprotective effect of plasmalogens (Pls) and explore the potential of lipid nanoparticles against neurodegenerative diseases. Our strategy aims to create a self-assembled system, enhancing the efficacy of plasmalogens and the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) for neuroprotection. The Pls, a distinctive group of membrane glycerophospholipids, typically contain a polyunsaturated fatty acyl chain at the sn-2 position and an alkyl chain linked by a vinyl-ether bond at the sn-1 position of the glycerol backbone. Pls, with their unique structure featuring a vinyl ether bond, possess free radical scavenging capabilities and antioxidant properties. Addressing the decline in plasmalogen levels in aging individuals holds promise for therapies related to Parkinson's disease, Alzheimer's disease, and dementia. Recent research has expanded our understanding of their antioxidant effects, anti-inflammation, and their involvement in ferroptosis. However, challenges persist in implementing plasmalogens in treatments of neurodegenerative diseases and in developing suitable drug delivery systems. We summarize the progress in lipid nanoparticles (LNPs) for targeting multiple neurodegeneration mechanisms. Our research on plasmalogen-loaded LNPs explores their fabrication mechanism and in vitro/in vivo impacts on neurodegenerative models. Our study shows the feasibility of enhancing Pls efficacy using LNPs as carriers. We employ natural plasmalogens from scallops to create nanoformulations involving a non-lamellar lipid excipient (MO) for structural stabilization, various surfactants, and small amounts of vitamin E, curcumin, or coenzyme Q10. Using small-angle X-ray scattering (SAXS), we identified the structural features of various LNPs (vesicles, cubosomes, and hexosomes). Our in vitro evaluations utilized human neuroblastoma SH-SY5Y cells, differentiated with 10 µM retinoic acid for 5 days. Cell viability tests indicated non-toxicity of the LNPs at a total lipid concentration of 10 µM for 24-hour incubation. We study the impact of Pls nanoparticles on an in vitro model of Parkinson's disease using neuronal cells induced by the neurotoxin 6-OHDA. Using the SH-SY5Y cell line, we explore cellular damage mechanisms (oxidative stress and apoptotic enzymes) via identifying the impact on the ERK-Akt-CREB-BDNF signaling pathway. Several documented neuroprotective compounds were used to demonstrate the ability to restore neuronal lesions caused by 6-OHDA, offering a model of neurodegenerative conditions to further elucidate the beneficial effects of the Pls-based LNPs. We then focus on the cAMP response element binding protein (CREB) and its phosphorylation leading to neurotrophin expression, crucial in preventing neurological disorders. Through lipid peptide nano-assemblies, we studied the impact of different structural organizations of the LNPs on CREB phosphorylation in an in vitro model of Parkinson's disease. Notably, liquid crystalline lipid nanoparticles loaded with plasmalogens prolonged CREB activation under neurodegenerative conditions, showing potential for enhanced neuroregeneration through sustained CREB activation in response to the neurotrophic nanoassemblies. In a mouse model of Parkinson's disease, vesicle and hexosome LNPs demonstrated distinct effectiveness in restoring motor function. The nanomedicine-mediated intervention influenced Parkinson's disease-related gene regulation and rebalanced lipid profiles. Nasal administration of Pls-loaded LNPs improved disease behavioral symptoms and downregulated genes like IL33 and Tnfa. The obtained results indicated the significant impact of hexosomal LNP nanomedicines on disease attenuation, lipid metabolism, and responsive gene modifications potentially involved in regeneration
Zussy, Charleine. "Caractérisation des effets de l'injection intracérébroventriculaire du peptide β-amyloïde [25-35] chez le rat mâle adulte : impact sur un système de neuroprotection endogène : le BDNF (Brain-derived neurotrophic factor) et ses récepteurs." Montpellier 2, 2009. http://www.theses.fr/2009MON20204.
Alzheimer's disease is a neurodegenerative pathology characterized by the presence of senile plaques. The major component of senile plaques is an amyloid-ß protein (Aβ). In this study, we assessed the time-course effects and regional changes observed after a single intracerebroventricular (icv) injection of aggregated Aβ fragment [25-35] (Aβ25-35; 10 µg/rat), on physiological parameters (body weight, general activity and body temperature), behavioral responses (spatial short- and long-term memories), stress parameters (BDNF and CORT levels, oxidative, inflammation, neuroprotection, cellular) and on histological parameters (neuroinflammation, acetylcholine systems, hippocampus integrity, BDNF system). We shown that a single icv injection of Aβ25-35 has a significant impact on short- and long-term memories, HPA axis activity, oxidative stress, brain level of a neuroprotective agent (BDNF) and its receptors (TrkB and p75), ER and mitochondrial stress, apoptotic processes, astrogliosis and microgliosis, cholinergic systems, hippocampus integrity and hippocampal neurogenesis. This study allows to realize the parallel existing between the effects induced by Aβ25-35 icv injection and numerous relevant signs of the pathology observed in patients. It seems that effects observed could be due to differential regulation of BDNF system on cerebral regions
Vaudry, David. "Contribution à l'étude des effets neurotrophiques du pituitary adenylate cyclase-activating polypeptide (PACAP) sur les cellules granulaires au cours du développement du cervelet de rat." Rouen, 2000. http://www.theses.fr/2000ROUES044.
Corbière, Auriane. "Etude du peptidome du cervelet de rat au cours du développement et identification des effets neurotrophiques de la nociceptine dans la mise en place des neurones en grain." Thesis, Normandie, 2017. http://www.theses.fr/2017NORMR063/document.
The cerebellum is a structure involved in many motor and cognitive functions whose development occurs after birth under the control of various factors, including neuropeptides. Peptides acting on cerebellar cortex development often exhibit a specific pattern of expression with in rodents a high expression over the 2 first postnatal weeks which then decreases at adulthood. The aim of this study was to identify additional peptides with such expression profile and to characterize their putative functions in the development of the cerebellar cortex and more particularly, in the establishment of cerebellar granule neurons which are the most abundant cells of the cerebellum. To address this, cerebella of rats aged from 8 to 90 days-old were analyzed by mass spectrometry. Among the 33 peptides identified in the cerebellum, 4 had the particular expression profile we were looking for. We choose to study further one of them, i.e. the nociceptin, and confirmed peptidomic results by measuring the expression of its gene precursor and of its receptor. Combining laser microdissection and qPCR approaches revealed that both nociceptin and its receptor genes were expressed in the internal granular layer of the cerebellar cortex. Functional studies showed that nociceptin exerts a neurotrophic effect on granule neurons by increasing their survival and differentiation, but had no effect on their motility. Preliminary in vivo experiments indicate that nociceptin can also counteract ethanol-induced toxicity. The last part of the present study aimed to identify new neuropeptides expressed in the rat cerebellum by using de novo sequencing. The large amount of peptide sequences initially found was then reduced to only 6 candidates for further analysis, by using filters such as recurrence of the sequences and their differential expression in between the four developmental stages considered. Additional genomic studies will help to decrease even further this number, in order to focus the biological tests on the targets which are most likely to code for biological active peptides