Готові списки джерел за темами / Neurotrophic peptide

Добірка наукової літератури з теми "Neurotrophic peptide"

Автор: Grafiati
Опубліковано: 7 липня 2024

Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями

Оберіть тип джерела:

Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "Neurotrophic peptide".

Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.

Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.

Зміст

  1. Статті в журналах
  2. Дисертації
  3. Книги
  4. Частини книг
  5. Тези доповідей конференцій

Статті в журналах з теми "Neurotrophic peptide":

1

Notaras, Michael, and Maarten van den Buuse. "Brain-Derived Neurotrophic Factor (BDNF): Novel Insights into Regulation and Genetic Variation." Neuroscientist 25, no. 5 (November 2, 2018): 434–54. http://dx.doi.org/10.1177/1073858418810142.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Since its discovery, brain-derived neurotrophic factor (BDNF) has spawned a literature that now spans 35 years of research. While all neurotrophins share considerable overlap in sequence homology and their processing, BDNF has become the most widely studied neurotrophin because of its broad roles in brain homeostasis, health, and disease. Although research on BDNF has produced thousands of articles, there remain numerous long-standing questions on aspects of BDNF molecular biology and signaling. Here we provide a comprehensive review, including both a historical narrative and a forward-looking perspective on advances in the actions of BDNF within the brain. We specifically review BDNF’s gene structure, peptide composition (including domains, posttranslational modifications and putative motif sites), mechanisms of transport, signaling pathway recruitment, and other recent developments including the functional effects of genetic variation and the discovery of a new BDNF prodomain ligand. This body of knowledge illustrates a highly conserved and complex role for BDNF within the brain, that promotes the idea that the neurotrophin biology of BDNF is diverse and that any disease involvement is likely to be equally multifarious.
2

Wetmore, C. J., Y. Cao, R. F. Pettersson, and L. Olson. "Brain-derived neurotrophic factor (BDNF) peptide antibodies: characterization using a Vaccinia virus expression system." Journal of Histochemistry & Cytochemistry 41, no. 4 (April 1993): 521–33. http://dx.doi.org/10.1177/41.4.8450192.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
We describe and characterize a series of polyclonal antibodies, generated against amino acid sequences unique to various regions within pro- and mature brain-derived neurotrophic factor (BDNF), a member of the highly conserved nerve growth factor (NGF) family of neurotrophins. Synthetic peptides were coupled to carrier proteins in the presence of glutaraldehyde to restrict the host animals' immune response to epitopes that are compatible with aldehyde fixation. Initial screenings of the reactivity of the antisera were made on brain sections processed for immunohistochemistry after peptide injections into brain parenchyma. As a means of further characterizing these peptide antisera, we have evaluated the reactivity and specificity of the peptide antibodies in BHK cells expressing recombinant pro- and mature BDNF protein from a T7 RNA polymerase-driven Vaccinia virus system. Several of the antibodies strongly stained components of cells transfected with the BDNF gene but did not label wild-type cells nor cells containing only the expression vector. It has also been possible to detect differential compartmentalization of the BDNF protein at various stages of processing in the BHK cells, as well as in situ in cryostat sections of brain tissue, with antisera to the pro- and mature protein. We conclude that several of our antisera recognize not only the specific peptide immunogens but also what appears to be the corresponding protein native to neurons.
3

Redigolo, Luigi, Vanessa Sanfilippo, Diego La Mendola, Giuseppe Forte, and Cristina Satriano. "Bioinspired Nanoplatforms Based on Graphene Oxide and Neurotrophin-Mimicking Peptides." Membranes 13, no. 5 (April 30, 2023): 489. http://dx.doi.org/10.3390/membranes13050489.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Neurotrophins (NTs), which are crucial for the functioning of the nervous system, are also known to regulate vascularization. Graphene-based materials may drive neural growth and differentiation, and, thus, have great potential in regenerative medicine. In this work, we scrutinized the nano–biointerface between the cell membrane and hybrids made of neurotrophin-mimicking peptides and graphene oxide (GO) assemblies (pep−GO), to exploit their potential in theranostics (i.e., therapy and imaging/diagnostics) for targeting neurodegenerative diseases (ND) as well as angiogenesis. The pep−GO systems were assembled via spontaneous physisorption onto GO nanosheets of the peptide sequences BDNF(1-12), NT3(1-13), and NGF(1-14), mimicking the brain-derived neurotrophic factor (BDNF), the neurotrophin 3 (NT3), and the nerve growth factor (NGF), respectively. The interaction of pep−GO nanoplatforms at the biointerface with artificial cell membranes was scrutinized both in 3D and 2D by utilizing model phospholipids self-assembled as small unilamellar vesicles (SUVs) or planar-supported lipid bilayers (SLBs), respectively. The experimental studies were paralleled via molecular dynamics (MD) computational analyses. Proof-of-work in vitro cellular experiments with undifferentiated neuroblastoma (SH-SY5Y), neuron-like, differentiated neuroblastoma (dSH-SY5Y), and human umbilical vein endothelial cells (HUVECs) were carried out to shed light on the capability of the pep−GO nanoplatforms to stimulate the neurite outgrowth as well as tubulogenesis and cell migration.
4

Longo, F. M., T. K. Vu, and W. C. Mobley. "The in vitro biological effect of nerve growth factor is inhibited by synthetic peptides." Cell Regulation 1, no. 2 (January 1990): 189–95. http://dx.doi.org/10.1091/mbc.1.2.189.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Nerve growth factor (NGF)1 is a neurotrophic polypeptide that acts via specific receptors to promote the survival and growth of neurons. To delineate the NGF domain(s) responsible for eliciting biological activity, we synthesized small peptides corresponding to three regions in NGF that are hydrophilic and highly conserved. Several peptides from mouse NGF region 26-40 inhibited the neurite-promoting effect of NGF on sensory neurons in vitro. Inhibition was sequence-specific and could be overcome by increasing the concentration of NGF. Moreover, peptide actions were specific for NGF-mediated events in that they failed to block the neurotrophic activity of ciliary neuronotrophic factor (CNTF) or phorbol 12-myristate 13-acetate (PMA). In spite of the inhibition of NGF activity, peptides did not affect the binding of radiolabeled NGF. These studies define one region of NGF that may be required for neurotrophic activity.
5

Baazaoui, Narjes, and Khalid Iqbal. "Alzheimer’s Disease: Challenges and a Therapeutic Opportunity to Treat It with a Neurotrophic Compound." Biomolecules 12, no. 10 (October 2, 2022): 1409. http://dx.doi.org/10.3390/biom12101409.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Alzheimer’s disease (AD) is a progressive neurodegenerative disease with an insidious onset and multifactorial nature. A deficit in neurogenesis and synaptic plasticity are considered the early pathological features associated with neurofibrillary tau and amyloid β pathologies andneuroinflammation. The imbalance of neurotrophic factors with an increase in FGF-2 level and a decrease in brain derived neurotrophic factor (BDNF) and neurotrophin 4 (NT-4) in the hippocampus, frontal cortex and parietal cortex and disruption of the brain micro-environment are other characteristics of AD. Neurotrophic factors are crucial in neuronal differentiation, maturation, and survival. Several attempts to use neurotrophic factors to treat AD were made, but these trials were halted due to their blood-brain barrier (BBB) impermeability, short-half-life, and severe side effects. In the present review we mainly focus on the major etiopathology features of AD and the use of a small neurotrophic and neurogenic peptide mimetic compound; P021 that was discovered in our laboratory and was found to overcome the difficulties faced in the administration of the whole neurotrophic factor proteins. We describe pre-clinical studies on P021 and its potential as a therapeutic drug for AD and related neurodegenerative disorders. Our study is limited because it focuses only on P021 and the relevant literature; a more thorough investigation is required to review studies on various therapeutic approaches and potential drugs that are emerging in the AD field.
6

Wang, Rong, Jing-Yan Zhang, Fang Yang, Zhi-Juan Ji, Goutam Chakraborty, and Shu-Li Sheng. "A novel neurotrophic peptide: APP63-73." NeuroReport 15, no. 17 (December 2004): 2677–80. http://dx.doi.org/10.1097/00001756-200412030-00025.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
7

Joliot, A., I. Le Roux, M. Volovitch, E. Bloch-Gallego, and A. Prochiantz. "Neurotrophic activity of a homeobox peptide." Progress in Neurobiology 42, no. 2 (February 1994): 309–11. http://dx.doi.org/10.1016/0301-0082(94)90070-1.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
8

Pittenger, Gary, and Aaron Vinik. "Nerve Growth Factor and Diabetic Neuropathy." Experimental Diabesity Research 4, no. 4 (2003): 271–85. http://dx.doi.org/10.1155/edr.2003.271.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Neuropathy is one of the most debilitating complications of both type 1 and type 2 diabetes, with estimates of prevalence between 50–90% depending on the means of detection. Diabetic neuropathies are heterogeneous and there is variable involvement of large myelinated fibers and small, thinly myelinated fibers. Many of the neuronal abnormalities in diabetes can be duplicated by experimental depletion of specific neurotrophic factors, their receptors or their binding proteins. In experimental models of diabetes there is a reduction in the availability of these growth factors, which may be a consequence of metabolic abnormalities, or may be independent of glycemic control. These neurotrophic factors are required for the maintenance of the neurons, the ability to resist apoptosis and regenerative capacity. The best studied of the neurotrophic factors is nerve growth factor (NGF) and the related members of the neurotrophin family of peptides. There is increasing evidence that there is a deficiency of NGF in diabetes, as well as the dependent neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) that may also contribute to the clinical symptoms resulting from small fiber dysfunction. Similarly, NT3 appears to be important for large fiber and IGFs for autonomic neuropathy. Whether the observed growth factor deficiencies are due to decreased synthesis, or functional, e.g. an inability to bind to their receptor, and/or abnormalities in nerve transport and processing, remains to be established. Although early studies in humans on the role of neurotrophic factors as a therapy for diabetic neuropathy have been unsuccessful, newer agents and the possibilities uncovered by further studies should fuel clinical trials for several generations. It seems reasonable to anticipate that neurotrophic factor therapy, specifically targeted at different nerve fiber populations, might enter the therapeutic armamentarium.
9

Sima, Anders A. F., Weixian Zhang, Zhen-guo Li, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Diabetic polyneuropathy (DPN) occurs more frequently in type 1 diabetes resulting in a more severe DPN. The differences in DPN between the two types of diabetes are due to differences in the availability of insulin and C-peptide. Insulin and C-peptide provide gene regulatory effects on neurotrophic factors with effects on axonal cytoskeletal proteins and nerve fiber integrity. A significant abnormality in type 1 DPN is nodal degeneration. In the type 1 BB/Wor-rat, C-peptide replacement corrects metabolic abnormalities ameliorating the acute nerve conduction defect. It corrects abnormalities of neurotrophic factors and the expression of neuroskeletal proteins with improvements of axonal size and function. C-peptide corrects the expression of nodal adhesive molecules with prevention and repair of the functionally significant nodal degeneration. Cognitive dysfunction is a recognized complication of type 1 diabetes, and is associated with impaired neurotrophic support and apoptotic neuronal loss. C-peptide prevents hippocampal apoptosis and cognitive deficits. It is therefore clear that substitution of C-peptide in type 1 diabetes has a multitude of effects on DPN and cognitive dysfunction. Here the effects of C-peptide replenishment will be extensively described as they pertain to DPN and diabetic encephalopathy, underpinning its beneficial effects on neurological complications in type 1 diabetes.
10

Mizui, 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, no. 23 (May 26, 2015): E3067—E3074. http://dx.doi.org/10.1073/pnas.1422336112.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Most growth factors are initially synthesized as precursor proteins and subsequently processed into their mature form by proteolytic cleavage, resulting in simultaneous removal of a pro-peptide. However, compared with that of mature form, the biological role of the pro-peptide is poorly understood. Here, we investigated the biological role of the pro-peptide of brain-derived neurotrophic factor (BDNF) and first showed that the pro-peptide is expressed and secreted in hippocampal tissues and cultures, respectively. Interestingly, we found that the BDNF pro-peptide directly facilitates hippocampal long-term depression (LTD), requiring the activation of GluN2B-containing NMDA receptors and the pan-neurotrophin receptor p75NTR. The BDNF pro-peptide also enhances NMDA-induced α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor endocytosis, a mechanism crucial for LTD expression. Thus, the BDNF pro-peptide is involved in synaptic plasticity that regulates a mechanism responsible for promoting LTD. The well-known BDNF polymorphism valine for methionine at amino acid position 66 (Val66Met) affects human memory function. Here, the BDNF pro-peptide with Met mutation completely inhibits hippocampal LTD. These findings demonstrate functional roles for the BDNF pro-peptide and a naturally occurring human BDNF polymorphism in hippocampal synaptic depression.
Більше джерел
Також вас можуть зацікавити розширені добірки на тему "Neurotrophic peptide" для конкретних типів джерел:
Статті в журналах Дисертації

Дисертації з теми "Neurotrophic peptide":

1

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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Trophic factors have shown great promise in their potential to treat neurological disease. In particular, glial cell line-derived neurotrophic factor (GDNF) has been identified as a potent neurotrophic factor for midbrain dopamine (DA) neurons in the substantia nigra (SN), which lose function in Parkinson’s disease (PD). GDNF progressed to phase II clinical trials, which did not meet proposed endpoints. The large size and binding characteristics of GDNF have been suspected to contribute to some of the shortcomings of GDNF related to delivery to target brain regions. Smaller peptides derived from GDNF (Dopamine-Neuron Stimulating Peptides – DNSPs) have been recently investigated and appear to demonstrate trophic-like effects comparable to GDNF. In the described studies, a time course study was conducted to determine in vivo DA-release characteristics 1-, 2- and 4- weeks after peptide treatment. These studies determined the effects on DA terminals within striatal sub-regions using microelectrodes. A heterogeneous effect on striatal sub-regions was apparent with the maximum effect in the dorsal striatum – corresponding to terminals originating from the SN. Dysregulation of GDNF or GDNF signaling is believed to contribute to motor dysfunction in aging and PD. Thus, it is hypothesized that GDNF is necessary for the maintenance and function of neurons. To extend this line of investigation, in vivo functional measures (DA-release and -uptake) and behavioral and cellular alterations were investigated in a transgenic mouse model (Gdnf+/-) with reduced GDNF protein levels. The described studies determined that both DA-uptake and -release properties were altered in middle-aged Gdnf+/- mice with only modest reductions in DA neurochemical levels. GDNF levels in Gdnf+/- mice were restored to levels comparable to wild-type (WT) counterparts by treatment with GDNF. GDNF protein supplementation led to enhanced motor behavior and increased markers for DA neurons in the SN of Gdnf+/- mice. Gdnf+/- mice appeared to show a heightened sensitivity to GDNF treatment compared to WT counterparts. Overall, this body of work examines novel synthetic peptides with potential to enhance DA-neuron function and expands upon the current understanding of GDNF’s role in the nigrostriatal pathway.
2

Kaska, 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/.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
3

Parikh, 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
4

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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
L'objectif principal de cette thèse est d'étudier l'effet neuroprotecteur des plasmalogènes (Pls) et d'explorer le potentiel des nanoparticules lipidiques contre les maladies neurodégénératives. Notre stratégie vise à créer un système auto-assemblé, augmentant l'efficacité des plasmalogènes et d'un neuropeptide, le polypeptide activateur de l'adénylate cyclase hypophysaire (PACAP), pour la neuroprotection. Pls, un groupe distinctif de glycérophospholipides membranaires, contiennent généralement une chaîne d'acyle gras polyinsaturé en position sn-2 et une chaîne alkyle liée par une liaison éther-vinyle en position sn-1 du squelette glycérol. La correction du déclin des niveaux de plasmalogènes chez les personnes âgées offre des perspectives pour les thérapies liées à la maladie de Parkinson, à la maladie d'Alzheimer et à la démence. Nous résumons les progrès des nanoparticules lipidiques (LNPs) dans le ciblage de multiples mécanismes de neurodégénérescence. Notre recherche sur les LNPs chargées en plasmalogène explore leur impact in vitro/in vivo sur des modèles de neurodégénérescence. Notre étude montre la faisabilité d'améliorer l'efficacité du Pls avec les LNPs. Nous utilisons des plasmalogènes naturels pour créer des nanoformulations impliquant un excipient lipidique nonlamellaire (monooléine, divers agents tensioactifs et de petites quantités de vitamine E, curcumine ou coenzyme Q10. En utilisant la méthode SAXS, nous avons identifié des caractéristiques structurelles des LNPs (vésicules, cubosomes et hexosomes). Les évaluations in vitro utilisent des cellules SH-SY5Y, différenciées avec 10 µM d'acide rétinoïque pendant 5 jours. Les tests de viabilité cellulaire indiquent une absente de toxicité à une concentration totale en lipides de 10 µM pour une incubation de 24 heures. Nous avons étudié l'impact des nanoparticules chargées en Pls sur les cellules neuronales en utilisant la neurotoxine 6-OHDA comme modèle in vitro de la maladie de Parkinson. Nous explorons les mécanismes de dommages cellulaires (stress oxydatif et enzymes apoptotiques), identifiant la voie de signalisation ERK-Akt-CREB-BDNF. Cela suggère la nécessité d'adopter plusieurs stratégies dans le traitement des maladies neurodégénératives. Plusieurs composés neuroprotecteurs documentés ont été utilisés pour démontrer la capacité à restaurer les lésions neuronales causées par le 6-OHDA, offrant un modèle de conditions neurodégénératives pour élucider davantage les effets bénéfiques des Pls. Nous nous concentrons ensuite sur la protéine de liaison à l'élément de réponse au cAMP (CREB) et sa phosphorylation conduisant à l'expression des neurotrophines, cruciale pour prévenir les troubles neurologiques. À travers des nano-assemblages lipidiques-peptiques, nous avons étudié l'impact des différentes organisations structurelles des LNPs sur la phosphorylation de CREB dans un modèle in vitro de la maladie de Parkinson. Dans un modèle murin de la maladie de Parkinson, les LNPs de structure vésiculaire et hexosomale ont démontré une efficacité distincte dans la restauration de la fonction motrice. L'intervention intranasale a influencé la régulation génétique liée à la maladie de Parkinson et rééquilibré les profils lipidiques. L'administration nasale de LNPs chargées en Pls a amélioré les symptômes comportementaux de la maladie et a régulé à la baisse des gènes tels que IL33 et Tnfa. Nos résultats indiquent l'impact significatif des nanoformulations hexosomales sur l'atténuation de la maladie, le métabolisme lipidique et les modifications génétiques réactives potentiellement impliquées dans la régénération
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
5

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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
Neuropeptides, such as substance P (SP) and bombesin/gastrin-releasing peptide (BN/GRP), and neurotrophins are involved in neuro-immunomodulatory processes and have marked trophic, growth-promoting and inflammation-modulating properties. The impact of these modulators in rheumatoid arthritis (RA) is, however, unclear. An involvement of the innervation, including the peptidergic innervation, is frequently proposed as an important factor for arthritic disease. Many patients with RA, but not all, benefit from treatment with anti-TNF medications. The studies presented here aimed to investigate the roles of neuropeptides, with an emphasis on BN/GRP and SP, and neurotrophins, especially with attention to brain-derived neurotrophic factor (BDNF), in human and murine knee joint tissue. The expression patterns of these substances and their receptors in synovial tissue from patients with either RA or osteoarthritis (OA) were studied in parallel with the levels of these factors in blood and synovial fluid from patients with RA and from healthy controls. Correlation studies were also performed comparing the levels of neuropeptides with those of pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6)]. Furthermore, the impact of anti-TNF treatment on the levels of BDNF in blood was investigated. In a murine model of RA, the expression of these substances on articular chondrocytes along with their expression in synovial tissue was investigated. The expression of BN/GRP in human synovial tissue was confined to fibroblast-like and mononuclear-like cells whereas SP was detected in nerve-related structures. Receptors for these neuropeptides (GRP-R and NK-1R) were frequently present in blood vessel walls, and on fibroblast-like and mononuclear-like cells. The expression of BDNF and its receptors, p75 neurotrophin receptor and TrkB, was mainly confined to nerve structures. The levels of SP, and particularly those of BN/GRP, in synovial fluid and peripheral blood correlated with the levels of pro-inflammatory cytokines. There were clearly more correlations between SP-BN/GRP and inflammatory parameters than between BDNF and these factors. Plasma levels of BDNF were decreased following anti-TNF-treatment. In the joints of the murine model, there was a marked expression of neurotrophins, neurotrophin receptors and NK-1R/GRP-R in the articular chondrocytes. The expression was down-regulated in the arthritic animals. A neurotrophin system was found to develop in the inflammatory infiltrates of the synovium in the arthritic mice. The results presented suggest that there is a local, and not nerve-related, supply of BN/GRP in the human synovial tissue. Furthermore, BN/GRP and SP have marked effects in the synovial tissue of patients with RA, i.e., there were abundant receptor expressions, and these neuropeptides are, together with cytokines, likely to be involved in the neuro-immunomodulation that occurs in arthritis. The observations do on the whole suggest that the neuropeptides, rather than BDNF, are related to inflammatory processes in the human knee joint. A new effect of anti-TNF treatment; i.e., lowering plasma levels of BDNF, was observed. Severe arthritis, as in the murine model, lead to a decrease in the levels of neurotrophin, and neurotrophin and neuropeptide receptor expressions in the articular cartilage. This fact might be a drawback for the function of the chondrocytes. Certain differences between the expression patterns in the synovial tissue of the murine model and those of human arthritic synovial tissue were noted. It is obvious that local productions in the synovial tissue, nerve-related supply in this tissue and productions in chondrocytes to different extents occur for the investigated substances.
6

Lim, 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
7

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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
La maladie d'Alzheimer (MA) est une pathologie neurodégénérative caractérisée par la présence de plaques séniles majoritairement composées par la protéine β-amyloïde (Aβ). Afin de caractériser les effets de la toxicité amyloïde, nous avons évalué l'impact au cours du temps d'une injection intracérébroventriculaire (icv) du peptide Aβ25-35 agrégé sur des paramètres comportementaux, physiologiques et biochimiques chez le rat et sur un système neuroprotecteur endogène, le BDNF. Nous avons caractérisé 1, 2, 3 et 6 sem après l'injection icv d'Aβ25-35, les effets sur la mémoire à court- et long-terme, sur les niveaux dans l'amygdale, le cortex frontal, l'hippocampe et l'hypothalamus du stress oxydant, des processus apoptotiques et du BDNF ainsi que ces récepteurs (TrkB et p75). Chez ces animaux, des études immunohistologiques sont également réalisées sur le système BDNF, la neuroinflammation, la neurogénèse et la perte cellulaire hippocampique. Cette étude montre que l'injection d'Aβ25-35 induit des déficits mnésiques, un stress oxydant, de la mitochondrie et du réticulum endoplasmique et des processus apoptotiques. L'Aβ25-35 a un impact sur le système cholinergique, l'intégrité hippocampique, la neurogénèse et la neuroinflammation. Les taux de corticostérone et le système BDNF sont également modifiés. L'injection icv d'Aβ25-35 induit les signes neuropathologiques majeurs de la MA chez le rat et valide ce modèle d'injection comme un bon modèle non-transgénique de la MA. De plus, il semble qu'une partie des effets observés pourraient être le résultat d'une dérégulation du système BDNF dans certaines régions du cerveau
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
8

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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Анотація:
BDNF/TrkB são descritos em diversas neoplasias onde iniciam sinais mitogênicos, facilitam o crescimento tumoral, previnem apoptose e regulam angiogênese e metástase. Outros fatores de crescimento também são importantes para tumorigênese, como GRP/GRPR e EGF/EGFR. O objetivo geral deste trabalho foi investigar o papel de BDNF/TrkB em câncer colorretal avaliando possíveis interações com GRPR e EGFR. Verificamos que BDNF e seu receptor, TrkB, estão presentes em amostras de pacientes com câncer colorretal esporádico, e os níveis de BDNF encontram-se mais elevados no tecido neoplásico que no tecido adjacente ao tumor. O tratamento com RC- 3095, um antagonista de GRPR, na linhagem celular de câncer colorretal humana, HT-29, causa diminuição nos níveis de NGF secretados pelas células e aumento de BDNF em relação ao controle não tratado. RC-3095 inibe a proliferação e viabilidade celular das linhagens HT-29 (EGFR positiva) e SW-620 (EGFR negativa), embora apenas em HT-29 ocorra um aumento significativo na expressão de mRNA de BDNF. Por isso, um anticorpo monoclonal anti-EGFR, cetuximabe, foi combinado a RC-3095, nas células HT-29, sendo capaz de prevenir tal aumento, sugerindo que este efeito seja mediado por EGFR. Os tratamentos com um inibidor de Trks, K252a (1000 nM) ou com cetuximabe (10 nM) também inibem a proliferação celular. Entretanto, a combinação de BDNF a cetuximabe previne este efeito, enquanto que a combinação de doses não efetivas de K252a (10 nM) à cetuximabe (1 nM) inibe a proliferação celular de HT- 29. Além disso, cetuximabe também causa aumento na expressão de mRNA de TrkB e BDNF, após 600 minutos de tratamento. Nossos resultados sugerem que a inibição da proliferação celular in vitro ou do crescimento tumoral in vivo devem acontecer através do bloqueio combinado entre GRPR e TrkB em células de câncer colorretal EGFR positivas, e que BDNF também esteja envolvido em mecanismos de resistência a fármacos. Por isso, o bloqueio de BDNF / TrkB pode emergir como potencial alvo antitumoral.
BDNF / 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.
9

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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
10

Kritz, 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
Більше джерел

Книги з теми "Neurotrophic peptide":

1

Rush, Robert A. Neurotrophin Protocols. Humana Press, 2013.

Знайти повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
2

Rush, Robert A. Neurotrophin Protocols. Humana Press, 2001.

Знайти повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.

Частини книг з теми "Neurotrophic peptide":

1

Facci, Laura, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
2

Bronzuoli, Maria Rosanna, Roberta Facchinetti, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
3

Facchinetti, Roberta, Maria Rosanna Bronzuoli, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
4

Windisch, M., A. Gschanes, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
5

Caban, Secil, Yılmaz Capan, Patrick Couvreur, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
6

Yemisci, Muge, Secil Caban, Eduardo Fernandez-Megia, Yilmaz Capan, Patrick Couvreur, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
7

Frim, David M., Julie K. Andersen, James M. Schumacher, M. Priscilla Short, Ole Isacson, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
8

Lapchak, Paul A., Dalia M. Araujo, Timothy L. Denton, Millicent M. Dugich-Djordjevic, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
9

Travaglia, A., and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.
10

Pan, Weihong, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.

Тези доповідей конференцій з теми "Neurotrophic peptide":

1

Akimov, Mikhail, Elena Fomina-Ageeva, Polina Dudina, Lyudmila Andreeva, Nikolaj Myasoedov, and 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.

Повний текст джерела
Стилі APA, Harvard, Vancouver, ISO та ін.

До бібліографії