Статті в журналах: "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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

11

Angelucci, Francesco, Francesca Gelfo, Marco Fiore, Nicoletta Croce, Aleksander A. Mathé, Sergio Bernardini, and Carlo Caltagirone. "The effect of neuropeptide Y on cell survival and neurotrophin expression in in-vitro models of Alzheimer’s disease." Canadian Journal of Physiology and Pharmacology 92, no. 8 (August 2014): 621–30. http://dx.doi.org/10.1139/cjpp-2014-0099.

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Alzheimer’s disease (AD) is a disorder characterized by the accumulation of abnormally folded protein fragments in neurons, i.e., β-amyloid (Aβ) and tau protein, leading to cell death. Several neuropeptides present in the central nervous system (CNS) are believed to be involved in the pathophysiology of AD. Among them, neuropeptide Y (NPY), a small peptide widely distributed throughout the brain, has generated interest because of its role in neuroprotection against excitotoxicity in animal models of AD. In addition, it has been shown that NPY modulates neurogenesis. Interestingly, these latter effects are similar to those elicited by neurotrophins, which are critical molecules for the function and survival of neurons that degenerate during the course of AD. In this review we summarize the evidence for the involvement of NPY and neurotrophins in AD pathogenesis, and the similarity between them in CNS neurons. Finally, we recapitulate our recent in-vitro evidence for the involvement of neurotrophin nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in the neuroprotective effect elicited by NPY in AD neuron-like models (neuroblastoma cells or primary cultures exposed to toxic concentrations of Aβ’s pathogenic fragment 25–35), and propose a putative mechanism based on NPY-induced inhibition of voltage-dependent Ca2+ influx in pre- and post-synaptic neurons.

12

Chohan, Muhammad Omar, Olga Bragina, Syed Faraz Kazim, Gloria Statom, Narjes Baazaoui, Denis Bragin, Khalid Iqbal, Edwin Nemoto, and Howard Yonas. "Enhancement of Neurogenesis and Memory by a Neurotrophic Peptide in Mild to Moderate Traumatic Brain Injury." Neurosurgery 76, no. 2 (September 24, 2014): 201–15. http://dx.doi.org/10.1227/neu.0000000000000577.

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ABSTRACT BACKGROUND: Traumatic brain injury (TBI) is a risk factor for Alzheimer disease (AD), a neurocognitive disorder with similar cellular abnormalities. We recently discovered a small molecule (Peptide 6) corresponding to an active region of human ciliary neurotrophic factor, with neurogenic and neurotrophic properties in mouse models of AD and Down syndrome. OBJECTIVE: To describe hippocampal abnormalities in a mouse model of mild to moderate TBI and their reversal by Peptide 6. METHODS: TBI was induced in adult C57Bl6 mice using controlled cortical impact with 1.5 mm of cortical penetration. The animals were treated with 50 nmol/d of Peptide 6 or saline solution for 30 days. Dentate gyrus neurogenesis, dendritic and synaptic density, and AD biomarkers were quantitatively analyzed, and behavioral tests were performed. RESULTS: Ipsilateral neuronal loss in CA1 and the parietal cortex and increase in Alzheimer-type hyperphosphorylated tau and A-β were seen in TBI mice. Compared with saline solution, Peptide 6 treatment increased the number of newborn neurons, but not uncommitted progenitor cells, in dentate gyrus by 80%. Peptide 6 treatment also reversed TBI-induced dendritic and synaptic density loss while increasing activity in tri-synaptic hippocampal circuitry, ultimately leading to improvement in memory recall on behavioral testing. CONCLUSION: Long-term treatment with Peptide 6 enhances the pool of newborn neurons in the dentate gyrus, prevents neuronal loss in CA1 and parietal cortex, preserves the dendritic and synaptic architecture in the hippocampus, and improves performance on a hippocampus-dependent memory task in TBI mice. These findings necessitate further inquiry into the therapeutic potential of small molecules based on neurotrophic factors.

13

Abdulla, Fuad A., Timothy D. Moran, Sridhar Balasubramanyan, and Peter A. Smith. "Effects and consequences of nerve injury on the electrical properties of sensory neurons." Canadian Journal of Physiology and Pharmacology 81, no. 7 (July 1, 2003): 663–82. http://dx.doi.org/10.1139/y03-064.

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Nociceptive pain alerts the body to potential or actual tissue damage. By contrast, neuropathic or "noninflammatory" pain, which results from injury to the nervous system, serves no useful purpose. It typically continues for years after the original injury has healed. Sciatic nerve lesions can invoke chronic neuropathic pain that is accompanied by persistent, spontaneous activity in primary afferent fibers. This activity, which reflects changes in the properties and functional expression of Na+, K+, and Ca2+ channels, initiates a further increase in the excitability of second-order sensory neurons in the dorsal horn. This change persists for many weeks. The source of origin of the pain thus moves from the peripheral to the central nervous system. We hypothesize that this centralization of pain involves the inappropriate release of peptidergic neuromodulators from primary afferent fibers. Peptides such as substance P, neuropeptide Y (NPY), calcitonin-gene-related peptide (CGRP), and brain-derived neurotrophic factor (BDNF) may promote enduring changes in excitability as a consequence of neurotrophic actions on ion channel expression in the dorsal horn. Findings that form the basis of this hypothesis are reviewed. Study of the neurotrophic control of ion channel expression by spinal peptides may thus provide new insights into the etiology of neuropathic pain.Key words: neuropathic pain, spinal cord injury, allodynia, dorsal root ganglion, axotomy.

14

Brenneman, D. E., E. A. Neale, G. A. Foster, S. W. d'Autremont, and G. L. Westbrook. "Nonneuronal cells mediate neurotrophic action of vasoactive intestinal peptide." Journal of Cell Biology 104, no. 6 (June 1, 1987): 1603–10. http://dx.doi.org/10.1083/jcb.104.6.1603.

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The developmental regulation of neuronal survival by vasoactive intestinal peptide (VIP) was investigated in dissociated spinal cord-dorsal root ganglion (SC-DRG) cultures. Previous studies demonstrated that VIP increased neuronal survival in SC-DRG cultures when synaptic transmission was blocked with tetrodotoxin (TTX). This effect was further investigated to determine if VIP acted directly on neurons or via nonneuronal cells. For these studies, SC-DRG cells were cultured under conditions designed to provide preparations enriched for a particular cell type: astrocyte-enriched background cell (BG) cultures, meningeal fibroblast cultures, standard mixed neuron-nonneuron (STD) cultures, and neuron-enriched (N) cultures. Addition of 0.1 nM VIP to TTX-treated STD cultures for 5 d prevented the TTX-mediated death and the death that occurred naturally during development in culture, whereas the same treatment on N cultures did not prevent neuronal cell death. Conditioned medium from VIP-stimulated BG cultures prevented neuronal cell death when added to the medium (10% of total volume) of N cultures treated with TTX. The same amount of conditioned medium from BG cultures that were not treated with VIP had no protective action on N cultures. Conditioned medium from N or meningeal fibroblast cultures, either with or without VIP treatment, did not prevent TTX-mediated cell death in N test cultures. These data indicate that VIP increases the availability of neurotrophic survival-promoting substances derived from nonneuronal cultures, the most likely source being astroglial cells. This study suggests that VIP has a role in mediating a neuron-glia-neuron interaction that influences the trophic regulation of neuronal survival.

15

Ishiguro, Mariko, Miyuki Murayama, Akira Oomori, and Tokiko Hama. "1412 A peptide which has neurotrophic factor-like activities." Neuroscience Research Supplements 18 (January 1993): S149. http://dx.doi.org/10.1016/s0921-8696(05)81094-1.

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16

Igase, Keiji, Seiji Matsuda, Jyunya Tanaka, and Masahiro Sakanaka. "1236 Neurotrophic activity of prosaposin 18-mer peptide fragment." Neuroscience Research 28 (January 1997): S160. http://dx.doi.org/10.1016/s0168-0102(97)90430-2.

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17

Sheng, Shu Li, Rong Wang, Zhi Quan Ji, Fang Yang, and Jing Yan Zhang. "Amyloid protein precursor 63–73 peptide sequence is neurotrophic." Neurobiology of Aging 21 (May 2000): 258. http://dx.doi.org/10.1016/s0197-4580(00)83113-9.

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18

Lee, Eun Hye, Seon Sook Kim, Seul Lee, Kwan-Hyuck Baek, and Su Ryeon Seo. "Pituitary Adenylate Cyclase-activating Polypeptide (PACAP) Targets Down Syndrome Candidate Region 1 (DSCR1/RCAN1) to control Neuronal Differentiation." Journal of Biological Chemistry 290, no. 34 (July 8, 2015): 21019–31. http://dx.doi.org/10.1074/jbc.m115.639476.

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Pituitary adenylate cyclase-activating peptide (PACAP) is a neurotrophic peptide involved in a wide range of nervous functions, including development, differentiation, and survival, and various aspects of learning and memory. Here we report that PACAP induces the expression of regulator of calcineurin 1 (RCAN1, also known as DSCR1), which is abnormally expressed in the brains of Down syndrome patients. Increased RCAN1 expression is accompanied by activation of the PKA-cAMP response element-binding protein pathways. EMSA and ChIP analyses demonstrate the presence of a functional cAMP response element in the RCAN1 promoter. Moreover, we show that PACAP-dependent neuronal differentiation is significantly disturbed by improper RCAN1 expression. Our data provide the first evidence of RCAN1, a Down syndrome-related gene, as a novel target for control of the neurotrophic function of PACAP.

19

Jarvis, C. R., Z. G. Xiong, J. R. Plant, D. Churchill, W. Y. Lu, B. A. Macvicar, and J. F. Macdonald. "Neurotrophin Modulation of NMDA Receptors in Cultured Murine and Isolated Rat Neurons." Journal of Neurophysiology 78, no. 5 (November 1, 1997): 2363–71. http://dx.doi.org/10.1152/jn.1997.78.5.2363.

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Jarvis, C. R., Z.-G. Xiong, J. R. Plant, D. Churchill, W.-Y. Lu, B. A. MacVicar, and J. F. MacDonald. Neurotrophin modulation of NMDA receptors in cultured murine and isolated rat neurons. J. Neurophysiol. 78: 2363–2371, 1997. Patch-clamp and calcium imaging techniques were used to assess the acute effects of the neurotrophins, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and nerve growth factor (NGF), on the responses of cultured and acutely isolated hippocampal and cultured striatal neurons to the glutamate receptor agonist N-methyl-d-aspartic acid (NMDA). The effects of BDNF on NMDA-activated currents were examined in greater detail. Currents evoked by NMDA, and the accompanying changes in intracellular calcium, were enhanced by low concentrations of the neurotrophins (1–20 ng/ml). The potentiation by the neurotrophins was rapid in onset and offset (<1 s). The neurotrophins also reduced desensitization of these currents in most cells. The enhancement of NMDA-activated currents by BDNF was observed using both perforated and whole cell patch recording techniques and could be demonstrated in outside-out patches. Furthermore, its effects were not attenuated by pretreatment with the protein kinase inhibitors genistein or 1-(5-isoquinolynesulfony)2-methylpiperazine (H7). Therefore, the actions of BDNF do not appear to be mediated by phosphorylation. Similar enhancements were observed with NT-3 and NT-4 and with NGF despite the fact that hippocampal neurons lack TrkA receptors. All together this evidence suggests that the enhancement of NMDA-evoked currents is unlikely to be mediated through the activation of growth factor receptors. Modulation of NMDA responses by BDNF was dependent on the concentration of extracellular glycine. The most pronounced potentiation by BDNF was observed at low concentrations, whereas no potentiation was observed in saturating concentrations of glycine, suggesting that BDNF may have increased the affinity of the NMDA receptor for glycine. However, the competitive glycine-site antagonist 7-chloro-kynurenic acid blocked the enhancement by BDNF without shifting the dose-inhibition relationship for this antagonist, and Mg2+ consistently depressed the potentiation of NMDA-evoked currents by BDNF, indicating that BDNF does not alter glycine affinity. BDNF also reversibly increased the probability of opening of NMDA channels recorded from outside-out patches taken from cultured hippocampal neurons. Other unrelated peptides including dynorphin and somatostatin also caused a glycine-dependent enhancement of NMDA currents and depressed the currents in saturating concentrations of glycine. In contrast, a shortened analogue dynorphin (6-17), which lacks N-terminus glycine residues, and another peptide met-enkephalin were without effects on NMDA currents recorded in low concentrations of glycine. Our results suggest that neurotrophins and other peptides can serve as glycine-like ligands for the NMDA receptor.

20

Dogrukol-Ak, Dilek, Vijaya B. Kumar, Jan S. Ryerse, Susan A. Farr, Sulekha Verma, Naoko Nonaka, Tomoya Nakamachi, et al. "Isolation of Peptide Transport System-6 from Brain Endothelial Cells: Therapeutic Effects with Antisense Inhibition in Alzheimer and Stroke Models." Journal of Cerebral Blood Flow & Metabolism 29, no. 2 (November 12, 2008): 411–22. http://dx.doi.org/10.1038/jcbfm.2008.131.

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By isolating for the first time ever a peptide transporter from the blood—brain barrier (BBB) and developing an antisense that selectively targets the brain-to-blood efflux component, we were able to deliver a therapeutic concentration of the neurotrophic peptide pituitary adenylate cyclase-activating polypeptide (PACAP) 27 to brain in animal models of Alzheimer's and stroke. Efflux pumps at the BBB are major causes of BBB impermeability to peptides. PACAP is neuroprotective in vitro in femtomole amounts, but brain uptake of PACAP27 is limited by an efflux component of peptide transport system-6 (PTS-6). Here, we characterized, isolated, and sequenced this component of PTS-6, identifying it as β-F1 ATPase, and colocalized it with PACAP27 on BBB endothelial cells. Antisenses targeting the BBB inhibited PACAP27 efflux, thus increasing brain uptake of PACAP27. Treatment with antisense +PACAP27 improved cognition in a mouse model of Alzheimer's disease and reduced infarct size after cerebral ischemia. This represents the first isolation from BBB tissue of a peptide transporter and shows that inhibition of peptide efflux pumps is a potential strategy for drug delivery to brain.

21

Magrì, Antonio, and Diego La Mendola. "Copper Binding Features of Tropomyosin-Receptor-Kinase-A Fragment: Clue for Neurotrophic Factors and Metals Link." International Journal of Molecular Sciences 19, no. 8 (August 12, 2018): 2374. http://dx.doi.org/10.3390/ijms19082374.

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The nerve growth factor (NGF) is a neurotrophin essential for the development and maintenance of neurons, whose activity is influenced by copper ions. The NGF protein exerts its action by binding to its specific receptor, TrkA. In this study, a specific domain of the TrkA receptor, region 58–64, was synthesized and its copper(II) complexes characterized by means of potentiometric and spectroscopic studies. The two vicinal histidine residues provide excellent metal anchoring sites and, at physiological pH, a complex with the involvement of the peptide backbone amide nitrogen is the predominant species. The TrkA peptide is competitive for metal binding with analogous peptides due to the N-terminal domain of NGF. These data provide cues for future exploration of the effect of metal ions on the activity of the NGF and its specific cellular receptor.

22

Liu, Xingyu, Haiyuan Ren, Ai Peng, Haoyang Cheng, Jiahao Chen, Xue Xia, Ting Liu, and Xiaojing Wang. "The Effect of RADA16-I and CDNF on Neurogenesis and Neuroprotection in Brain Ischemia-Reperfusion Injury." International Journal of Molecular Sciences 23, no. 3 (January 27, 2022): 1436. http://dx.doi.org/10.3390/ijms23031436.

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Scaffold materials, neurotrophic factors, and seed cells are three elements of neural tissue engineering. As well-known self-assembling peptide-based hydrogels, RADA16-I and modified peptides are attractive matrices for neural tissue engineering. In addition to its neuroprotective effects, cerebral dopamine neurotrophic factor (CDNF) has been reported to promote the proliferation, migration, and differentiation of neural stem cells (NSCs). However, the role of RADA16-I combined with CDNF on NSCs remains unknown. First, the effect of RADA16-I hydrogel and CDNF on the proliferation and differentiation of cultured NSCs was investigated. Next, RADA16-I hydrogel and CDNF were microinjected into the lateral ventricle (LV) of middle cerebral artery occlusion (MCAO) rats to activate endogenous NSCs. CDNF promoted the proliferation of NSCs, while RADA16-I induced the neural differentiation of NSCs in vitro. Importantly, both RADA16-I and CDNF promoted the proliferation, migration, and differentiation of endogenous NSCs by activating the ERK1/2 and STAT3 pathways, and CDNF exerted an obvious neuroprotective effect on brain ischemia-reperfusion injury. These findings provide new information regarding the application of the scaffold material RADA16-I hydrogel and the neurotrophic factor CDNF in neural tissue engineering and suggest that RADA16-I hydrogel and CDNF microinjection may represent a novel therapeutic strategy for the treatment of stroke.

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Lu, Jiaju, Xun Sun, Heyong Yin, Xuezhen Shen, Shuhui Yang, Yu Wang, Wenli Jiang, et al. "A neurotrophic peptide-functionalized self-assembling peptide nanofiber hydrogel enhances rat sciatic nerve regeneration." Nano Research 11, no. 9 (March 17, 2018): 4599–613. http://dx.doi.org/10.1007/s12274-018-2041-9.

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O'Leary, Paul D., and Richard A. Hughes. "Design of Potent Peptide Mimetics of Brain-derived Neurotrophic Factor." Journal of Biological Chemistry 278, no. 28 (May 2, 2003): 25738–44. http://dx.doi.org/10.1074/jbc.m303209200.

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Valk, Gerlof D., Arnoud C. Kappelle, Aim�e M. L. Tjon-A-Tsien, Bert Bravenboer, Karel Bakker, Robert P. J. Michels, Cees M. Groenhout, and Frederik W. Bertelsmann. "Treatment of diabetic polyneuropathy with the neurotrophic peptide ORG 2766." Journal of Neurology 243, no. 3 (1996): 257–63. http://dx.doi.org/10.1007/bf00868523.

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Yao, Jie, Lina Ma, Rong Wang, Shuli Sheng, Zhijuan Ji, and Jingyan Zhang. "Neurotrophic effects of amyloid precursor protein peptide 165 in vitro." Brain Research Bulletin 120 (January 2016): 58–62. http://dx.doi.org/10.1016/j.brainresbull.2015.11.005.

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Kim, Inhyeok, Yonjae Kim, Daewoong Kang, Junyang Jung, Sungsoo Kim, Hwasung Rim, Sanghoon Kim, and Seung-Geun Yeo. "Neuropeptides Involved in Facial Nerve Regeneration." Biomedicines 9, no. 11 (October 29, 2021): 1575. http://dx.doi.org/10.3390/biomedicines9111575.

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Neuropeptides and neurotransmitters act as intermediaries to transmit impulses from one neuron to another via a synapse. These neuropeptides are also related to nerve degeneration and regeneration during nerve damage. Although there are various neuropeptides, three are associated with neural regeneration in facial nerve damage: calcitonin gene-related peptide (CGRP), galanin, and pituitary adenylyl cyclase-activating peptide (PACAP). Alpha CGRP in facial motoneurons is a signaling factor involved in neuroglial and neuromuscular interactions during regeneration. Thus, it may be a marker for facial nerve regeneration. Galanin is a marker of injured axons rather than nerve regeneration. PACAP has various effects on nerve regeneration by regulating the surrounding cells and providing neurotrophic factors. Thus, it may also be used as a marker for facial nerve regeneration. However, the precise roles of these substances in nerve generation are not yet fully understood. Animal studies have demonstrated that they may act as neuromodulators to promote neurotrophic factors involved in nerve regeneration as they appear early, before changes in the injured cells and their environment. Therefore, they may be markers of nerve regeneration.

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Williams, Gareth, Gareth Williams, Francisco Molina-Holgado, Francisco Molina-Holgado, Patrick Doherty, and Patrick Doherty. "Tandem Repeat Peptide Strategy for the Design of Neurotrophic Factor Mimetics." CNS & Neurological Disorders - Drug Targets 7, no. 1 (February 1, 2008): 110–19. http://dx.doi.org/10.2174/187152708783885200.

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Gozes, Illana, and Irit Spivak-Pohis. "Neurotrophic Effects of the Peptide NAP: A Novel Neuroprotective Drug Candidate." Current Alzheimer Research 3, no. 3 (July 1, 2006): 197–99. http://dx.doi.org/10.2174/156720506777632790.

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Grundke-Iqbal, Inge, M. Omar Chohan, Bin Li, Julie Blanchard, and Khalid Iqbal. "O4-04-08: Improvement of cognition with a neurogenic/neurotrophic peptide." Alzheimer's & Dementia 4 (July 2008): T193. http://dx.doi.org/10.1016/j.jalz.2008.05.534.

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BRENNEMAN, DOUGLAS E., TERRY M. PHILLIPS, BARRY W. FESTOFF, and ILLANA GOZES. "Identity of Neurotrophic Molecules Released from Astroglia by Vasoactive Intestinal Peptide." Annals of the New York Academy of Sciences 814, no. 1 Neuropeptides (April 1997): 167–73. http://dx.doi.org/10.1111/j.1749-6632.1997.tb46155.x.

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Brenneman, Douglas E., T. Nicol, D. Warren, and L. M. Bowers. "Vasoactive intestinal peptide: A neurotrophic releasing agent and an astroglial mitogen." Journal of Neuroscience Research 25, no. 3 (March 1990): 386–94. http://dx.doi.org/10.1002/jnr.490250316.

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Candalija, Ana, Thomas Scior, Hans-Richard Rackwitz, Jordan E. Ruiz-Castelan, Ygnacio Martinez-Laguna, and José Aguilera. "Interaction between a Novel Oligopeptide Fragment of the Human Neurotrophin Receptor TrkB Ectodomain D5 and the C-Terminal Fragment of Tetanus Neurotoxin." Molecules 26, no. 13 (June 30, 2021): 3988. http://dx.doi.org/10.3390/molecules26133988.

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This article presents experimental evidence and computed molecular models of a potential interaction between receptor domain D5 of TrkB with the carboxyl-terminal domain of tetanus neurotoxin (Hc-TeNT). Computational simulations of a novel small cyclic oligopeptide are designed, synthesized, and tested for possible tetanus neurotoxin-D5 interaction. A hot spot of this protein-protein interaction is identified in analogy to the hitherto known crystal structures of the complex between neurotrophin and D5. Hc-TeNT activates the neurotrophin receptors, as well as its downstream signaling pathways, inducing neuroprotection in different stress cellular models. Based on these premises, we propose the Trk receptor family as potential proteic affinity receptors for TeNT. In vitro, Hc-TeNT binds to a synthetic TrkB-derived peptide and acts similar to an agonist ligand for TrkB, resulting in phosphorylation of the receptor. These properties are weakened by the mutagenesis of three residues of the predicted interaction region in Hc-TeNT. It also competes with Brain-derived neurotrophic factor, a native binder to human TrkB, for the binding to neural membranes, and for uptake in TrkB-positive vesicles. In addition, both molecules are located together in vivo at neuromuscular junctions and in motor neurons.

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Liu, Jing, Pu Chen, Hongdong Song, Pengxiao Zhang, Man Wang, Zhenliang Sun, and Xiao Guan. "Prediction of Cholecystokinin-Secretory Peptides Using Bidirectional Long Short-term Memory Model Based on Transfer Learning and Hierarchical Attention Network Mechanism." Biomolecules 13, no. 9 (September 11, 2023): 1372. http://dx.doi.org/10.3390/biom13091372.

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Cholecystokinin (CCK) can make the human body feel full and has neurotrophic and anti-inflammatory effects. It is beneficial in treating obesity, Parkinson’s disease, pancreatic cancer, and cholangiocarcinoma. Traditional biological experiments are costly and time-consuming when it comes to finding and identifying novel CCK-secretory peptides, and there is an urgent need to develop a new computational method to predict new CCK-secretory peptides. This study combines the transfer learning method with the SMILES enumeration data augmentation strategy to solve the data scarcity problem. It establishes a fusion model of the hierarchical attention network (HAN) and bidirectional long short-term memory (BiLSTM), which fully extracts peptide chain features to predict CCK-secretory peptides efficiently. The average accuracy of the proposed method in this study is 95.99%, with an AUC of 98.07%. The experimental results show that the proposed method is significantly superior to other comparative methods in accuracy and robustness. Therefore, this method is expected to be applied to the preliminary screening of CCK-secretory peptides.

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Liu, Mingchuan, Shengjie Yang, Jinping Yang, Yita Lee, Junping Kou, and Chaojih Wang. "Neuroprotective and Memory-Enhancing Effects of Antioxidant Peptide From Walnut (Juglans regia L.) Protein Hydrolysates." Natural Product Communications 14, no. 7 (July 2019): 1934578X1986583. http://dx.doi.org/10.1177/1934578x19865838.

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Peptides have been reported to possess interesting biological properties. The present study was designed to evaluate neuroprotective and memory-enhancing effects of antioxidant peptide from walnut ( Juglans regia L.) protein hydrolysates. The neuroprotective effect of walnut peptide (WP) against oxidative stress on PC12 cells was evaluated. And zebrafish was used as the model to corroborate the effect. Its effect on learning and memory of mice using the Morris water maze and the step-down passive avoidance tests were performed. Moreover, the acute toxicity of WP was carried out to assess its safety profile. It was found that WP was able to suppress H2O2-induced cell death in PC12 cells. In the zebrafish model, WP had an obvious neuroprotective effect, and the ratio reached 42% at 222 µg/mL. The mechanism study revealed that WP could inhibit the activity of caspases 3/7 and 8, reduce the mRNA expression levels of Bax and glial cell line-derived neurotrophic factor, and improve the mRNA expression level of brain-derived neurotrophic factor significantly. Besides, the treatment of mice with WP shortened the escape latency and exhibited much longer target time and more crossing times significantly, compared with untreated control groups in the Morris water maze test. Similarly, the step-down passive avoidance test showed that WP could ameliorate memory impairments. The administrated dose (20.1 g/kg body weight [BW]) did not produce mortality or treatment-related adverse effects with regard to BW, general behavior, or relative organ weights of the tested male and female mice. The current results indicated that WP could exert neuroprotective effect, and attenuated learning and memory impairments. These ameliorating effects of WP may be useful for treatment of memory impairment in Alzheimer’s and its related diseases.

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Storey, A. T., and D. J. Kenny. "Growth, Development, and Aging of Orofacial Tissues: Neural Aspects." Advances in Dental Research 3, no. 1 (May 1989): 14–29. http://dx.doi.org/10.1177/08959374890030010101.

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Neural factors influence post-natal growth, development, and aging throughout the body. This influence may be mediated through sensory or motor effects interacting with endocrine and immunological factors. Growth effects may be expressed directly by sensory or motor nerves on the tissue or indirectly by motor function. Direct neurotrophic effects have been well-documented in the development of striated muscle, the taste bud, and the amphibian limb. Evidence for a trigeminal neurotrophic effect on tooth development and facial development is lacking. Growth disturbances of the jaws consequent to lesioning of the trigeminal nerve are due most likely to functional disturbances rather than neurotrophism. Examples of function impact on orofacial growth are abundant. Oral and facial target tissues, like those elsewhere in the body, determine the nature of the target tissue innervation and its central organization. Central effects consequent to tooth loss or dental pulp entirpation are well-documented. Inflammation and pain may exert growth effects through release of "wound hormones" or secondarily to somatic and autonomic effects. There is evidence that vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) elaborated from sympathetic and parasympathetic neurons may have a modulatory role in growth. While the effects of longstanding motor pathologies on skeletal growth are well-known, concomitant sensory deficits and soft tissue disturbances have not been examined. However, the pathological models beg the question of normal regulation. While muscle develops in the absence of innervation, neurotrophic effects are clearly identified. Little is known about the interaction of simple and complex motor behavior on growth. Regulation of growth is frequently visualized within a form-function paradigm. For example, anterior open bites have been seen as the consequence of tongue thrusting or tongue thrusting as a consequence of open bites. Low tonic forces in posture are thought to be more important in the development of both the face and the dental alveolar complex than the higher intermittent forces in mastication and swallowing. The need for an active (reflex) contribution to growth at the TMJ is in dispute. The specific chemical regulators of bone cartilage and soft tissue growth identified elsewhere in the body probably act in a similar fashion in orofacial development. The lack of chemical regulators common to both lists of growth factors and putative and demonstrated neural transmitters suggests that most post-natal growth regulation is secondary to function. Short- and long-term strategies are offered to address questions suitable for immediate and future investigation.

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Ekberg, Karin, and Bo-Lennart Johansson. "Effect of C-Peptide on Diabetic Neuropathy in Patients with Type 1 Diabetes." Experimental Diabetes Research 2008 (2008): 1–5. http://dx.doi.org/10.1155/2008/457912.

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Recent results indicate that proinsulin C-peptide, contrary to previous views, exerts important physiological effects and shows the characteristics of a bioactive peptide. Studies in type 1 diabetes, involving animal models as well as patients, demonstrate that C-peptide in replacement doses has the ability to improve peripheral nerve function and prevent or reverse the development of nerve structural abnormalities. Peripheral nerve function, as evaluated by determination of sensory nerve conduction velocity and quantitative sensory testing, is improved by C-peptide replacement in diabetes type 1 patients with early stage neuropathy. Similarly, autonomic nerve dysfunction is ameliorated following administration of C peptide for up to 3 months. As evaluated in animal models of type 1 diabetes, the improved nerve function is accompanied by reversal or prevention of nerve structural changes, and the mechanisms of action are related to the ability of C-peptide to correct diabetes-induced reductions in endoneurial blood flow and in -ATPase activity and modulation of neurotrophic factors. Combining the results demonstrates that C-peptide may be a possible new treatment of neuropathy in type 1 diabetes.

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Ju, Da-Tong, Ashok Kumar K., Wei-Wen Kuo, Tsung-Jung Ho, Ruey-Lin Chang, Wan-Teng Lin, Cecilia Hsuan Day, V. Vijaya Padma Viswanadha, Po-Hsiang Liao, and Chih-Yang Huang. "Bioactive Peptide VHVV Upregulates the Long-Term Memory-Related Biomarkers in Adult Spontaneously Hypertensive Rats." International Journal of Molecular Sciences 20, no. 12 (June 23, 2019): 3069. http://dx.doi.org/10.3390/ijms20123069.

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Hypertension is one of the growing risk factors for the progression of long-term memory loss. Hypertension-mediated memory loss and treatment remain not thoroughly elucidated to date. Plant-based natural compounds are an alternative solution to treating human diseases without side effects associated with commercial drugs. This study reveals that bioactive peptides extracted from soy hydrolysates mimic hypertension-mediated memory loss and neuronal degeneration and alters the memory molecular pathway in spontaneously hypertensive rats (SHR). The SHR animal model was treated with bioactive peptide VHVV (10 mg/kg/oral administration) and angiotensin-converting-enzyme (ACE) inhibitors (5 mg/kg/oral administration) for 24 weeks. We evaluated molecular level expression of brain-derived neurotrophic factor (BDNF), cAMP response element binding protein (CREB), and survival markers phospho-protein kinase B (P-AKT) and phosphoinositide 3-kinase (PI3K) after 24 weeks of treatment for SHR in this study. Western blotting, hematoxylin and eosin (H&E) staining, and immunohistochemistry showed long-term memory loss and neuronal degeneration in SHR animals. Bioactive peptide VHVV-treated animals upregulated the expression of long-term memory-relate proteins and neuronal survival. Spontaneously hypertensive rats treated with oral administration of bioactive peptide VHVV had activated CREB-mediated downstream proteins which may reduce hypertension-mediated long-term memory loss and maintain neuronal survival.

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Gul, Huseyin Fatih, Caner Yildirim, Can Emre Erdogan, Ozlem Gul та Nazlı Koc. "The Role of Galanin, Alarin, Irisin, PGC1-Α and BDNF in the Pathophysiology of Alzheimer's disease". International Journal of Medical Science and Clinical Invention 8, № 06 (27 червня 2021): 5498–507. http://dx.doi.org/10.18535/ijmsci/v8i06.09.

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The roles of novel peptides such as peroxisome proliferator-activated receptor gamma coactivator 1- alpha (PGC1-α), irisin, brain-derived neurotrophic factor (BDNF), galanin and alarin in Alzheimer's disease (AD) are not fully known. It was aimed to plasma levels of the novel peptides that may affect the pathophysiology of AD were examined. This study was conducted as a cross-sectional. The study consisted of two groups, including 45 newly diagnosed individuals with AD and 45 healthy individuals. The peptide levels in plasma samples collected from the groups were measured by the ELISA method. The mean plasma peptide levels and age differences, between the groups, and the correlations between them were analyzed by the statistically. The means ages of both groups were over 65 years old. When plasma PGC1-α, irisin, BDNF, galanin, and alarin levels between the groups were examined, decreases were found in the group with AD (3.56±0.79ng/mL, 16.33±4.07ng/mL, 3.36±1.47ng/mL, 13.93±4.24ng/L, 31.99±11.89pg/mL, respectively) compared to the control group (4.23±1.31ng/mL, 22.19±9.61ng/mL, 4.58±2.10ng/mL, 14.4±9.01ng/L, 54.93±15.80pg/mL, respectively). In the negative correlations observed between age and plasma peptide levels. Significant positive correlations were observed between plasma PGC1-α levels and irisin, alarin, and BDNF, and the significant positive correlations were also observed between plasma BDNF levels and irisin and alarin. As far as we know, the study is the first report in which the peptides mentioned in AD were examined together. We consider that more detailed studies are needed to shed light on the roles and mechanisms of these peptides in AD.

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Kim, Sokho, Jihye Choi, and Jungkee Kwon. "Thymosin Beta 4 Protects Hippocampal Neuronal Cells against PrP (106–126) via Neurotrophic Factor Signaling." Molecules 28, no. 9 (May 6, 2023): 3920. http://dx.doi.org/10.3390/molecules28093920.

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Prion protein peptide (PrP) has demonstrated neurotoxicity in brain cells, resulting in the progression of prion diseases with spongiform degenerative, amyloidogenic, and aggregative properties. Thymosin beta 4 (Tβ4) plays a role in the nervous system and may be related to motility, axonal enlargement, differentiation, neurite outgrowth, and proliferation. However, no studies about the effects of Tβ4 on prion disease have been performed yet. In the present study, we investigated the protective effect of Tβ4 against synthetic PrP (106–126) and considered possible mechanisms. Hippocampal neuronal HT22 cells were treated with Tβ4 and PrP (106–126) for 24 h. Tβ4 significantly reversed cell viability and reactive oxidative species (ROS) affected by PrP (106–126). Apoptotic proteins induced by PrP (106–126) were reduced by Tβ4. Interestingly, a balance of neurotrophic factors (nerve growth factor and brain-derived neurotrophic factor) and receptors (nerve growth factor receptor p75, tropomyosin related kinase A and B) were competitively maintained by Tβ4 through receptors reacting to PrP (106–126). Our results demonstrate that Tβ4 protects neuronal cells against PrP (106–126) neurotoxicity via the interaction of neurotrophic factors/receptors.

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Priestley, J. V., G. J. Michael, S. Averill, M. Liu, and N. Willmott. "Regulation of nociceptive neurons by nerve growth factor and glial cell line derived neurotrophic factor." Canadian Journal of Physiology and Pharmacology 80, no. 5 (May 1, 2002): 495–505. http://dx.doi.org/10.1139/y02-034.

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Nociceptive dorsal root ganglion (DRG) cells can be divided into three main populations, namely (1) small diameter non-peptide-expressing cells, (2) small-diameter peptide-expressing (calcitonin gene related peptide (CGRP), substance P) cells, and (3) medium-diameter peptide-expressing (CGRP) cells. The properties of these cell populations will be reviewed, with a special emphasis on the expression of the vanilloid (capsaicin) receptor VR1 and its regulation by growth factors. Cells in populations 1 and 2 express VR1, a nonselective channel that transduces certain nociceptive stimuli and that is crucial to the functioning of polymodal nociceptors. Cells in population 1 can be regulated by glial cell line derived neurotrophic factor (GDNF) and those in populations 2 and 3 by nerve growth factor (NGF). In vivo, DRG cells express a range of levels of VR1 expression and VR1 is downregulated after axotomy. However, treatment with NGF or GDNF can prevent this downregulation. In vitro, DRG cells also show a range of VR1 expression levels that is NGF and (or) GDNF dependent. Functional studies indicate that freshly dissociated cells also show differences in sensitivity to capsaicin. The significance of this is not known but may indicate a difference in the physiological role of cells in populations 1 and 2.Key words: nociceptors, CGRP, IB4, vanilloid, dorsal root ganglion.

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Xiao, Junhua, Richard A. Hughes, Joe Y. Lim, Agnes W. Wong, Jason J. Ivanusic, Anita H. Ferner, Trevor J. Kilpatrick, and Simon S. Murray. "A small peptide mimetic of brain-derived neurotrophic factor promotes peripheral myelination." Journal of Neurochemistry 125, no. 3 (February 24, 2013): 386–98. http://dx.doi.org/10.1111/jnc.12168.

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Yue, Mengyun, Jing Wei, Wenjie Chen, Daojun Hong, Tingtao Chen, and Xin Fang. "Neurotrophic Role of the Next-Generation Probiotic Strain L. lactis MG1363-pMG36e-GLP-1 on Parkinson’s Disease via Inhibiting Ferroptosis." Nutrients 14, no. 22 (November 18, 2022): 4886. http://dx.doi.org/10.3390/nu14224886.

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Parkinson’s disease (PD) is a neurodegenerative disease (NDD) with high and ongoing morbidity, bringing heavy burdens to PD patients seriously. Finding neurotrophic drugs still remains vital due to the limited drug spectrum available currently. Substantial evidence suggests that glucagon-like peptide 1 (GLP-1) exerts neuroprotection on PD, yet the short-lived biological activity markedly hindered its application. Herein, we investigated the neurotrophic role of the next-generation probiotic strain L. lactis MG1363-pMG36e-GLP-1 in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice and elucidated the mechanisms. Our data suggested that L. lactis MG1363-pMG36e-GLP-1 markedly enhanced motor deficits induced by MPTP via rescuing dopaminergic (DAergic) neurodegeneration in substantia nigra (SN). We found that L. lactis MG1363-pMG36e-GLP-1 exerts neurotrophic effects via activating the Keap1/Nrf2/GPX4 signalling pathway to down-regulate ACSL4 and up-regulate FSP1 to suppress ferroptosis. Additionally, the decreased oxidative stress levels via suppressing generations of ROS and MDA supported our findings. Lastly, we identified that the L. lactis MG1363-pMG36e-GLP-1 administration reversed dysbiosis in PD mice by increasing Akkermansia, Oscillospira, and Sutterella at the genus level. These results indicated that the neurotrophic effects of the next-generation probiotics L. lactis MG1363-pMG36e-GLP-1 against MPTP-induced Parkinsonism are mediated by modulating oxidative stress, inhibiting ferroptosis, and redressing dysbiosis.

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Safruddin, Khairu Zein, Ardhin Martdana, Fenska Seipalla, and Tirza Sosanta. "Organoruthenium 9E1 and APL Altered Collagen II263-272 Peptide as Therapy for Autoimmune Diseases." Journal of Health Science and Medical Therapy 1, no. 02 (September 28, 2023): 61–70. http://dx.doi.org/10.59653/jhsmt.v1i02.277.

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Therapy for autoimmune diseases such as rheumatoid arthritis and multiple sclerosis (MS) is currently available in symptom management, pain-relieving, and mitigation of disease. Currently, prescribed drugs for patients with the disease work in specific mechanisms, regardless of failure to determine the most effective medication. We use a literature review to highlight two newly examined substances: organoruthenium 9E1 and APL altered collagen II263-272 peptide, and elaborate substances mentioned above' potential to be used in rheumatoid arthritis and MS therapy. Several studies show positive effects from 9E1 and altered CII263-272 peptides on experimented mice. Altered CII263-272 peptide can elicit Th cells to produce neurotrophic factors, decrease the body amount of pro-inflammatory T cells, increase the body amount of anti-inflammatory T cells, and alleviate collagen-induced arthritis symptoms. Meanwhile, 9E1 can inhibit Mst1 kinase effectively (IC50=45nM), giving consequences of decreasing Th1 cells' cytokines, increasing Th2 cells' cytokines, decreasing body amount's IgG1 and IgG2a, slowing down EAE and collagen-induced arthritis' manifestation, increasing IL-10 and IL-4-producing T cells. Organoruthenium and altered CII263-272 peptide possess positive and multiple effects as therapies for EAE and collagen-induced arthritis, hence potential to be prescribed to patients with rheumatoid arthritis and MS. This literature review suggests further research concerning 9E1 and altered CII263-272 peptide usage in the community to examine their effectivity, side effects, and suitable dose.

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Lim, Juhee, Seokhee Kim, Changhyun Lee, Jeongwoo Park, Gabsik Yang, and Taehan Yook. "Verbenalin Reduces Amyloid-Beta Peptide Generation in Cellular and Animal Models of Alzheimer’s Disease." Molecules 27, no. 24 (December 8, 2022): 8678. http://dx.doi.org/10.3390/molecules27248678.

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Verbenalin, among the major constituents of Verbena officinalis, has been reported to exhibit sleep-promoting and antioxidant activities. This study demonstrates the effects of verbenalin on amyloid-beta (Aβ) peptide generation in Swedish mutant amyloid precursor protein (APP)-overexpressing Neuro2a cells (SweAPP/N2a) and in Alzheimer’s disease (AD) animal models. We further performed molecular biological analyses of these in vitro and in vivo models of AD. The effects of verbenalin were assessed based on the expression of factors related to Aβ peptide production using Western blotting, enzyme-linked immunosorbent assay, and immunohistochemistry (IHC). The intracellular expression and release of APP protein were both decreased by verbenalin treatment in SweAPP/N2a cells. Thus, the production of Aβ peptides was decreased. Compared to those in AD transgenic (Tg) mice, IHC revealed that verbenalin-treated animals showed decreased Aβ and tau expression levels in the hippocampus. In addition, verbenalin restored the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus of AD animal models. These findings suggest that verbenalin may decrease Aβ formation both in vitro and in vivo. Verbenalin may also help improve the pathological hallmarks of AD.

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Naletova, Irina, Cristina Satriano, Adriana Pietropaolo, Fiorenza Gianì, Giuseppe Pandini, Viviana Triaca, Giuseppina Amadoro, et al. "The Copper(II)-Assisted Connection between NGF and BDNF by Means of Nerve Growth Factor-Mimicking Short Peptides." Cells 8, no. 4 (April 1, 2019): 301. http://dx.doi.org/10.3390/cells8040301.

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Nerve growth factor (NGF) is a protein necessary for development and maintenance of the sympathetic and sensory nervous systems. We have previously shown that the NGF N-terminus peptide NGF(1-14) is sufficient to activate TrkA signaling pathways essential for neuronal survival and to induce an increase in brain-derived neurotrophic factor (BDNF) expression. Cu2+ ions played a critical role in the modulation of the biological activity of NGF(1-14). Using computational, spectroscopic, and biochemical techniques, here we report on the ability of a newly synthesized peptide named d-NGF(1-15), which is the dimeric form of NGF(1-14), to interact with TrkA. We found that d-NGF(1-15) interacts with the TrkA-D5 domain and induces the activation of its signaling pathways. Copper binding to d-NGF(1-15) stabilizes the secondary structure of the peptides, suggesting a strengthening of the noncovalent interactions that allow for the molecular recognition of D5 domain of TrkA and the activation of the signaling pathways. Intriguingly, the signaling cascade induced by the NGF peptides ultimately involves cAMP response element-binding protein (CREB) activation and an increase in BDNF protein level, in keeping with our previous result showing an increase of BDNF mRNA. All these promising connections can pave the way for developing interesting novel drugs for neurodegenerative diseases.

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Igase, Keiji, Junya Tanaka, Yoshiaki Kumon, Bo Zhang, Yasutaka Sadamoto, Nobuji Maeda, Saburo Sakaki, and Masahiro Sakanaka. "An 18-Mer Peptide Fragment of Prosaposin Ameliorates Place Navigation Disability, Cortical Infarction, and Retrograde Thalamic Degeneration in Rats with Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 19, no. 3 (March 1999): 298–306. http://dx.doi.org/10.1097/00004647-199903000-00008.

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It was previously reported that prosaposin possesses neurotrophic activity that is ascribed to an 18-mer peptide comprising the hydrophilic sequence of the rat saposin C domain. To evaluate the effect of the 18-mer peptide on ischemic neuronal damage, the peptide was infused in the left lateral ventricle immediately after occlusion of the left middle cerebral artery (MCA) in stroke-prone spontaneously hypertensive (SP-SH) rats. The treatment ameliorated the ischemia-induced space navigation disability and cortical infarction and prevented secondary thalamic degeneration in a dose-dependent manner. In culture experiments, treatment with the 18-mer peptide attenuated free radical-induced neuronal injury at low concentrations (0.002 to 2 pg/mL), and the peptide at higher concentrations (0.2 to 20 ng/mL) protected neurons against hypoxic insult. Furthermore, a saposin C fragment comprising the 18-mer peptide bound to synaptosomal fractions of the cerebral cortex, and this binding decreased at the 1st day after MCA occlusion and recovered to the preischemic level at the 7th day after ischemia. These findings suggest that the 18-mer peptide ameliorates neuronal damage in vivo and in vitro through binding to the functional receptor, although the cDNA encoding prosaposin receptor has not been determined yet.

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Fournier, J., P. E. Keane, P. Ferrara, and P. Soubrié. "SR 57746A: An Orally Active Non-Peptide Compound with Neurotrophic and Neuroprotective Effects." CNS Drug Reviews 3, no. 2 (June 1997): 148–67. http://dx.doi.org/10.1111/j.1527-3458.1997.tb00321.x.

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Glazner, Gordon W., Andre Boland, Albert E. Dresse, Douglas E. Brenneman, Illana Gozes, and Mark P. Mattson. "Activity-Dependent Neurotrophic Factor Peptide (ADNF9) Protects Neurons Against Oxidative Stress-Induced Death." Journal of Neurochemistry 73, no. 6 (January 18, 2002): 2341–47. http://dx.doi.org/10.1046/j.1471-4159.1999.0732341.x.

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50

Wong, Agnes W., Lauren Giuffrida, Rhiannon Wood, Haley Peckham, David Gonsalvez, Simon S. Murray, Richard A. Hughes, and Junhua Xiao. "TDP6, a brain-derived neurotrophic factor-based trkB peptide mimetic, promotes oligodendrocyte myelination." Molecular and Cellular Neuroscience 63 (November 2014): 132–40. http://dx.doi.org/10.1016/j.mcn.2014.10.002.

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