Auswahl der wissenschaftlichen Literatur zum Thema „Neurotrophic peptide“
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Zeitschriftenartikel zum Thema "Neurotrophic peptide"
Notaras, Michael, und Maarten van den Buuse. „Brain-Derived Neurotrophic Factor (BDNF): Novel Insights into Regulation and Genetic Variation“. Neuroscientist 25, Nr. 5 (02.11.2018): 434–54. http://dx.doi.org/10.1177/1073858418810142.
Der volle Inhalt der QuelleWetmore, C. J., Y. Cao, R. F. Pettersson und L. Olson. „Brain-derived neurotrophic factor (BDNF) peptide antibodies: characterization using a Vaccinia virus expression system.“ Journal of Histochemistry & Cytochemistry 41, Nr. 4 (April 1993): 521–33. http://dx.doi.org/10.1177/41.4.8450192.
Der volle Inhalt der QuelleRedigolo, Luigi, Vanessa Sanfilippo, Diego La Mendola, Giuseppe Forte und Cristina Satriano. „Bioinspired Nanoplatforms Based on Graphene Oxide and Neurotrophin-Mimicking Peptides“. Membranes 13, Nr. 5 (30.04.2023): 489. http://dx.doi.org/10.3390/membranes13050489.
Der volle Inhalt der QuelleLongo, F. M., T. K. Vu und W. C. Mobley. „The in vitro biological effect of nerve growth factor is inhibited by synthetic peptides.“ Cell Regulation 1, Nr. 2 (Januar 1990): 189–95. http://dx.doi.org/10.1091/mbc.1.2.189.
Der volle Inhalt der QuelleBaazaoui, Narjes, und Khalid Iqbal. „Alzheimer’s Disease: Challenges and a Therapeutic Opportunity to Treat It with a Neurotrophic Compound“. Biomolecules 12, Nr. 10 (02.10.2022): 1409. http://dx.doi.org/10.3390/biom12101409.
Der volle Inhalt der QuelleWang, Rong, Jing-Yan Zhang, Fang Yang, Zhi-Juan Ji, Goutam Chakraborty und Shu-Li Sheng. „A novel neurotrophic peptide: APP63-73“. NeuroReport 15, Nr. 17 (Dezember 2004): 2677–80. http://dx.doi.org/10.1097/00001756-200412030-00025.
Der volle Inhalt der QuelleJoliot, A., I. Le Roux, M. Volovitch, E. Bloch-Gallego und A. Prochiantz. „Neurotrophic activity of a homeobox peptide“. Progress in Neurobiology 42, Nr. 2 (Februar 1994): 309–11. http://dx.doi.org/10.1016/0301-0082(94)90070-1.
Der volle Inhalt der QuellePittenger, Gary, und Aaron Vinik. „Nerve Growth Factor and Diabetic Neuropathy“. Experimental Diabesity Research 4, Nr. 4 (2003): 271–85. http://dx.doi.org/10.1155/edr.2003.271.
Der volle Inhalt der QuelleSima, Anders A. F., Weixian Zhang, Zhen-guo Li und Hideki Kamiya. „The Effects of C-peptide on Type 1 Diabetic Polyneuropathies and Encephalopathy in the BB/Wor-rat“. Experimental Diabetes Research 2008 (2008): 1–13. http://dx.doi.org/10.1155/2008/230458.
Der volle Inhalt der QuelleMizui, Toshiyuki, Yasuyuki Ishikawa, Haruko Kumanogoh, Maria Lume, Tomoya Matsumoto, Tomoko Hara, Shigeto Yamawaki et al. „BDNF pro-peptide actions facilitate hippocampal LTD and are altered by the common BDNF polymorphism Val66Met“. Proceedings of the National Academy of Sciences 112, Nr. 23 (26.05.2015): E3067—E3074. http://dx.doi.org/10.1073/pnas.1422336112.
Der volle Inhalt der QuelleDissertationen zum Thema "Neurotrophic peptide"
Littrell, Ofelia Meagan. „NIGROSTRIATAL DOPAMINE-NEURON FUNCTION FROM NEUROTROPHIC-LIKE PEPTIDE TREATMENT AND NEUROTROPHIC FACTOR DEPLETION“. UKnowledge, 2011. http://uknowledge.uky.edu/neurobio_etds/1.
Der volle Inhalt der QuelleKaska, Jennifer Lynn. „Ependymin Mechanism of Action: Full Length EPN VS Peptide CMX-8933“. Link to electronic thesis, 2003. http://www.wpi.edu/Pubs/ETD/Available/etd-0528103-102730/.
Der volle Inhalt der QuelleParikh, Suchi Vipin. „Ependymin peptide mimetics that assuage ischemic damage increase gene expression of the anti-oxidative enzyme SOD“. Link to electronic thesis, 2003. http://www.wpi.edu/Pubs/ETD/Available/etd-0429103-132144.
Der volle Inhalt der QuelleWu, 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.
Der volle Inhalt der QuelleThe 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
Grimsholm, Ola. „Neuropeptides and neurotrophins in arthritis : studies on the human and mouse knee joint“. Doctoral thesis, Umeå universitet, Integrativ medicinsk biologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1863.
Der volle Inhalt der QuelleLim, Robyn Renata. „Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP) : peptide neurotrophic actions in comparison with those of nerve growth factor (NGF) on rat adrenal pheochromocytoma PC12 cells“. Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627532.
Der volle Inhalt der QuelleZussy, 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.
Der volle Inhalt der QuelleAlzheimer'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
Farias, Caroline Brunetto de. „BDNF/TrkB em câncer colorretal : interações funcionais com GRPR e EGFR“. reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2012. http://hdl.handle.net/10183/72306.
Der volle Inhalt der QuelleBDNF / TrkB are described in various cancers where they participate in tumor growth, apoptosis, angiogenesis and metastasis. Furthermore, other growth factors are also important to tumorigenesis as GRP/GRPR and EGF/EGFR. Therefore, the aim of this study was to investigate the role of BDNF/TrkB in colorectal cancer evaluating the interactions with GRPR and EGFR. We found that BDNF and its receptor, TrkB, are present in samples from patients diagnosed with sporadic colorectal cancer, and BDNF levels were higher in tumor tissue compared to adjacent tumor tissue. Treatment with RC-3095, GRPR antagonist, in human colorectal cancer cell line, HT-29 caused a decrease in NGF levels secreted by cells, and generated increase of BDNF when compared to untreated control. RC-3095 inhibited the proliferation and cell viability in HT-29 (EGFR positive) and SW-620 (EGFR negative), but only HT-29 cells showed a significant increase in BDNF mRNA expression. Therefore, a monoclonal anti-EGFR antibody, cetuximab was combined with RC-3095 in HT-29 cells, and was able to prevent such an increase, suggesting that this effect is mediated by EGFR. The treatment with a Trk inhibitor, K252a (1000 nM) or cetuximab (10 nM), inhibited cell proliferation. However, the combination of BDNF with cetuximab prevented this effect, whereas the combination of ineffective doses of K252a (10 nM) with cetuximab (1 nM) still inhibited cell proliferation of HT-29. Furthermore, cetuximab also caused an increase in BDNF and TrkB mRNA expression, 600 minutes after treatment. In summary, our results suggest that inhibition of cell proliferation in vitro or tumor growth in vivo must occur between the combination of GRPR and TrkB in EGFR positive colorectal cancer cells, and that BDNF is also involved in drug resistance mechanisms. Therefore, blockage of BDNF / TrkB may emerge as potential antitumor target.
Dyer, Jason Kim. „Presence of melanocortin receptors in Schwann cells in culture & functional relevance to the neurotrophic response : with an appendix on the establishment & characterisation of a new rat Schwann cell line“. Thesis, University of Bristol, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238825.
Der volle Inhalt der QuelleKritz, Angelika. „Peptides from phage display libraries for targeted gene delivery via the p75 neurotrophic receptor“. Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408712.
Der volle Inhalt der QuelleBücher zum Thema "Neurotrophic peptide"
Rush, Robert A. Neurotrophin Protocols. Humana Press, 2013.
Den vollen Inhalt der Quelle findenNeurotrophin Protocols. Humana Press, 2001.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Neurotrophic peptide"
Facci, Laura, und Stephen D. Skaper. „Amyloid β-Peptide Neurotoxicity Assay Using Cultured Rat Cortical Neurons“. In Neurotrophic Factors, 57–65. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-536-7_6.
Der volle Inhalt der QuelleBronzuoli, Maria Rosanna, Roberta Facchinetti und Caterina Scuderi. „Preparation of Rat Hippocampal Organotypic Cultures and Application to Study Amyloid β-Peptide Toxicity“. In Neurotrophic Factors, 333–41. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_24.
Der volle Inhalt der QuelleFacchinetti, Roberta, Maria Rosanna Bronzuoli und Caterina Scuderi. „An Animal Model of Alzheimer Disease Based on the Intrahippocampal Injection of Amyloid β-Peptide (1–42)“. In Neurotrophic Factors, 343–52. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_25.
Der volle Inhalt der QuelleWindisch, M., A. Gschanes und B. Hutter-Paier. „Neurotrophic activities and therapeutic experience with a brain derived peptide preparation“. In Journal of Neural Transmission. Supplementa, 289–98. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6467-9_25.
Der volle Inhalt der QuelleCaban, Secil, Yılmaz Capan, Patrick Couvreur und Turgay Dalkara. „Preparation and Characterization of Biocompatible Chitosan Nanoparticles for Targeted Brain Delivery of Peptides“. In Neurotrophic Factors, 321–32. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-536-7_27.
Der volle Inhalt der QuelleYemisci, Muge, Secil Caban, Eduardo Fernandez-Megia, Yilmaz Capan, Patrick Couvreur und Turgay Dalkara. „Preparation and Characterization of Biocompatible Chitosan Nanoparticles for Targeted Brain Delivery of Peptides“. In Neurotrophic Factors, 443–54. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_36.
Der volle Inhalt der QuelleFrim, David M., Julie K. Andersen, James M. Schumacher, M. Priscilla Short, Ole Isacson und Xandra Breakefield. „Gene Transfer into the Central Nervous System: Neurotrophic Factors“. In Growth Factors, Peptides and Receptors, 83–91. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2846-3_9.
Der volle Inhalt der QuelleLapchak, Paul A., Dalia M. Araujo, Timothy L. Denton, Millicent M. Dugich-Djordjevic und Franz Hefti. „Neurotrophins in the Adult Brain: Effects on Hippocampal Cholinergic Function Following Deafferentation, and Regulation of Their Expression by Pharmacological Agents and Lesions“. In Growth Factors, Peptides and Receptors, 241–53. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2846-3_23.
Der volle Inhalt der QuelleTravaglia, A., und D. La Mendola. „Zinc Interactions With Brain-Derived Neurotrophic Factor and Related Peptide Fragments“. In Vitamins and Hormones, 29–56. Elsevier, 2017. http://dx.doi.org/10.1016/bs.vh.2016.10.005.
Der volle Inhalt der QuellePan, Weihong, und Abba J. Kastin. „Neurotrophic Peptides“. In Handbook of Biologically Active Peptides, 1682–87. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-385095-9.00230-x.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Neurotrophic peptide"
Akimov, Mikhail, Elena Fomina-Ageeva, Polina Dudina, Lyudmila Andreeva, Nikolaj Myasoedov und Vladimir Bezuglov. „PRO-PROLIFERATIVE AND NEURO-PROTECTIVE ACTION OF THE NEUROTROPIC PEPTIDE FRWGPGP - SYNTHETIC ANALOGUE OF MELANOCORTINE PEPTIDE ACTH (6-9)“. In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m907.sudak.ns2020-16/56-57.
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