Готові списки джерел за темами / Chronic neuroinflammation

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Добірка наукової літератури з теми "Chronic neuroinflammation"

Автор: Grafiati

Опубліковано: 23 вересня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "Chronic neuroinflammation"

Vergne-Salle, Pascale, and Philippe Bertin. "Chronic pain and neuroinflammation." Joint Bone Spine 88, no. 6 (December 2021): 105222. http://dx.doi.org/10.1016/j.jbspin.2021.105222.

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Chen, Shih-Heng, Shuangyu Han, Chih-Fen Hu, Ran Zhou, Yun Gao, Dezhen Tu, Huiming Gao, et al. "Activation of the MAC1-ERK1/2-NOX2 Pathway Is Required for LPS-Induced Sustaining Reactive Microgliosis, Chronic Neuroinflammation and Neurodegeneration." Antioxidants 11, no. 6 (June 20, 2022): 1202. http://dx.doi.org/10.3390/antiox11061202.

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Recent studies suggest that improper resolution of acute neuroinflammation may lead to long-lasting low-grade chronic neuroinflammation and drive progressive neurodegeneration. However, the molecular mechanism underlying the transition from acute to chronic neuroinflammation remains unclear. The main purpose of this study was to search for potential pathways mediating LPS-elicited chronic neuroinflammation and resultant neurodegeneration. Using microglia cultures prepared from C57BL/6J, MAC1-deficient, and MyD88-deficient mice, the initial study showed that activation of TLR-4 is not sufficient for maintaining chronic neuroinflammation despite its essential role in LPS-initiated acute neuroinflammation. Opposite to TLR-4, our studies showed significantly reduced intensity of chronic neuroinflammation, oxidative stress, and progressive loss of nigral dopaminergic neurons in MAC1-deficient neuron/glial cultures or mice stimulated with LPS. Mechanistic studies revealed the essential role ERK1/2 activation in chronic neuroinflammation-elicited neurodegeneration, which was demonstrated by using an ERK1/2 inhibitor in neuron-glial cultures. Taken together, we propose a key role of the MAC1-NOX2-ERK1/2 signaling pathway in the initiation and maintenance of low-grade chronic neuroinflammation. Continuing ERK1/2 phosphorylation and NOX2 activation form a vicious feedforward cycle in microglia to maintain the low-grade neuroinflammation and drive neurodegeneration.

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Aloisi, Francesca, Sandra Columba-Cabezas, Diego Franciotta, Barbara Rosicarelli, Roberta Magliozzi, Richard Reynolds, Elena Ambrosini, Eliana Coccia, Marco Salvetti, and Barbara Serafini. "Lymphoid chemokines in chronic neuroinflammation." Journal of Neuroimmunology 198, no. 1-2 (July 2008): 106–12. http://dx.doi.org/10.1016/j.jneuroim.2008.04.025.

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Ji, Ru-Rong, Andrea Nackley, Yul Huh, Niccolò Terrando, and William Maixner. "Neuroinflammation and Central Sensitization in Chronic and Widespread Pain." Anesthesiology 129, no. 2 (August 1, 2018): 343–66. http://dx.doi.org/10.1097/aln.0000000000002130.

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Abstract Chronic pain is maintained in part by central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is also driven by neuroinflammation in the peripheral and central nervous system. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines. Recent studies suggest that central cytokines and chemokines are powerful neuromodulators and play a sufficient role in inducing hyperalgesia and allodynia after central nervous system administration. Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites. Thus, neuroinflammation drives widespread chronic pain via central sensitization. We also discuss sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain.

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Driessen, Alexandria K., Anna-Claire Devlin, Fionnuala T. Lundy, S. Lorraine Martin, Gerard P. Sergeant, Stuart B. Mazzone, and Lorcan P. McGarvey. "Perspectives on neuroinflammation contributing to chronic cough." European Respiratory Journal 56, no. 4 (July 9, 2020): 2000758. http://dx.doi.org/10.1183/13993003.00758-2020.

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Chronic cough can be a troublesome clinical problem. Current thinking is that increased activity and/or enhanced sensitivity of the peripheral and central neural pathways mediates chronic cough via processes similar to those associated with the development of chronic pain. While inflammation is widely thought to be involved in the development of chronic cough, the true mechanisms causing altered neural activity and sensitisation remain largely unknown. In this back-to-basics perspective article we explore evidence that inflammation in chronic cough may, at least in part, involve neuroinflammation orchestrated by glial cells of the nervous system. We summarise the extensive evidence for the role of both peripheral and central glial cells in chronic pain, and hypothesise that the commonalities between pain and cough pathogenesis and clinical presentation warrant investigations into the neuroinflammatory mechanisms that contribute to chronic cough. We open the debate that glial cells may represent an underappreciated therapeutic target for controlling troublesome cough in disease.

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Persidsky, Yuri, Jeremy Hill, Ming Zhang, Holly Dykstra, Malika Winfield, Nancy L. Reichenbach, Raghava Potula, Abir Mukherjee, Servio H. Ramirez, and Slava Rom. "Dysfunction of brain pericytes in chronic neuroinflammation." Journal of Cerebral Blood Flow & Metabolism 36, no. 4 (September 30, 2015): 794–807. http://dx.doi.org/10.1177/0271678x15606149.

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Brain pericytes are uniquely positioned within the neurovascular unit to provide support to blood brain barrier (BBB) maintenance. Neurologic conditions, such as HIV-1-associated neurocognitive disorder, are associated with BBB compromise due to chronic inflammation. Little is known about pericyte dysfunction during HIV-1 infection. We found decreased expression of pericyte markers in human brains from HIV-1-infected patients (even those on antiretroviral therapy). Using primary human brain pericytes, we assessed expression of pericyte markers (α1-integrin, α-smooth muscle actin, platelet-derived growth factor-B receptor β, CX-43) and found their downregulation after treatment with tumor necrosis factor-α (TNFα) or interleukin-1 β (IL-1β). Pericyte exposure to virus or cytokines resulted in decreased secretion of factors promoting BBB formation (angiopoietin-1, transforming growth factor-β1) and mRNA for basement membrane components. TNFα and IL-1β enhanced expression of adhesion molecules in pericytes paralleling increased monocyte adhesion to pericytes. Monocyte migration across BBB models composed of human brain endothelial cells and pericytes demonstrated a diminished rate in baseline migration compared to constructs composed only of brain endothelial cells. However, exposure to the relevant chemokine, CCL2, enhanced the magnitude of monocyte migration when compared to BBB models composed of brain endothelial cells only. These data suggest an important role of pericytes in BBB regulation in neuroinflammation.

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Ji, Ru-Rong, Zhen-Zhong Xu, and Yong-Jing Gao. "Emerging targets in neuroinflammation-driven chronic pain." Nature Reviews Drug Discovery 13, no. 7 (June 20, 2014): 533–48. http://dx.doi.org/10.1038/nrd4334.

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Delery, Elizabeth C., and Andrew G. MacLean. "Chronic Viral Neuroinflammation: Speculation on Underlying Mechanisms." Viral Immunology 32, no. 1 (February 2019): 55–62. http://dx.doi.org/10.1089/vim.2018.0093.

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Kirk, S. L., and S. J. Karlik. "VEGF and vascular changes in chronic neuroinflammation." Journal of Autoimmunity 21, no. 4 (December 2003): 353–63. http://dx.doi.org/10.1016/s0896-8411(03)00139-2.

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Mawey, Feytie Magda, Azimatul Karimah, Erlyn Limoa, and Muhammad Nazmuddin. "Neuroinflammation in Schizophrenia." Jurnal Psikiatri Surabaya 10, no. 1 (May 31, 2021): 1. http://dx.doi.org/10.20473/jps.v10i1.20871.

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Schizophrenia is a chronic debilitating mental illness. In many aspects, the neuropathology of schizophrenia is closely associated with neuroinflammation, especially microglial activation. Microglial hyperactivity, which is characterized by the predominant release of proinflammatory cytokines serves as the basis of the neuroinflammation hypothesis in schizophrenia. The enhanced inflammatory induce neuronal susceptibility to oxidative stress and trigger, glutamatergic synaptic dysregulation, especially in the mesolimbic and mesocortical pathways. Many in vitro studies, in vivo animal evidence, post-mortem examinations, neuroimaging evaluations with Positron Emission Tomography (PET), anti-inflammatory and antipsychotic use converge upon the central role of microglial activation and proinflammatory cytokines as common of features schizophrenia.

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Дисертації з теми "Chronic neuroinflammation"

Marriott, Lisa Katherine. "Gonadal hormone modulation of chronic neuroinflammation." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280524.

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Post-menopausal women have an increased incidence of Alzheimer's disease (AD) that may be delayed in onset by estrogen replacement therapy (ERT). Estrogen has many neuroprotective and neurotrophic proclivities; therefore, its decline with menopause may leave the brain vulnerable to toxic insults stemming from disease states. Recent clinical trials investigating ERT as a treatment for AD found beneficial effects following short-term treatment that become attenuated, and possibly reversed, following longer treatment intervals. This doctoral dissertation examined the interaction of two conditions known to exist within the female AD brain: the presence of chronic neuroinflammation and either estrogen deprivation or chronic ERT. As the duration of treatment and regimen of estrogen administration may alter the effectiveness of ERT, chronic and fluctuating administration of estrogen were assessed against the behavioral, biochemical and pathological consequences of short- and long-term neuroinflammation in the female rat brain. Overall, the results suggest a strong interaction between neuroendocrine and autonomic function in the female brain with neuroinflammation. In the presence of chronic neuroinflammation, the brain differentially responds depending on the hormone status of the animal. Cognitive performance is impaired with neuroinflammation or constant estrogen; the combined occurrence of both conditions worsened performance more than either condition presented alone. However, gonadally intact females with neuroinflammation were unimpaired on the task and had approximately half the number of activated microglia. The pattern of activated microglia is unique to the female brain and highlights an interesting distribution not seen in male rats. Specifically, an elegant map of activated microglia emerges of brain areas involved in autonomic control, stress regulation and energy homeostasis. Regions showing the densest distribution of activated microglia are important autonomic relay stations that interconnect various brain regions conveying internal state information. Moreover, these regions have extensive bi-directional communication with both endocrine and immune systems, suggesting an extensive interaction occurring in the female brain capable of influencing multiple systems, including hormone secretion, sympathetic output, immune function and behavioral processes. This dissertation proposes that the interactions between these systems have important consequences for post-menopausal women with AD and are likely to underlie the varying effects seen with ERT.

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Hopp, Sarah Christine. "Microglia and calcium dysregulation during chronic neuroinflammation and aging:causes and consequences." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1414416679.

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Bros, Esqueu Maria Elena [Verfasser]. "Mitochondrial damage and axon degeneration in chronic neuroinflammation / Maria Elena Bros Esqueu." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1100387625/34.

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Infante, Duarte Carmen [Verfasser]. "Antigen-independent pathogenic and protective immunity in chronic neuroinflammation / Carmen Infante Duarte." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1043480854/34.

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Peruzzotti-Jametti, Luca. "Neural stem cells respond to extracellular succinate via SUCNR1/GPR91 to ameliorate chronic neuroinflammation." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/277000.

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Neural stem cell (NSC) transplantation induces recovery in animal models of central nervous system (CNS) diseases, in part by modulating adaptive and innate immune responses. Since metabolism governs the phenotype and function of immune cells, the aim of this thesis was to investigate whether NSCs have the ability to regulate the immunometabolic components underpinning neuroinflammation. Herein I have identified a new mechanism by which transplanted somatic and directly-induced NSCs counteract CNS-compartmentalised chronic inflammation in mice. NSC transplantation reduces the immunometabolite succinate in the cerebrospinal fluid, while decreasing the burden of mononuclear phagocyte (MP) infiltration and secondary CNS damage. Mechanistically, the anti-inflammatory activity of NSCs arises in response to succinate released by inflammatory MPs, which activates succinate receptor 1 (SUCNR1)/GPR91 on NSCs, thus initiating prostaglandin E2 secretion and extracellular succinate scavenging. This work uncovers a succinate-SUCNR1 axis in NSCs that clarifies how stem cells respond to inflammatory metabolic signals to inhibit the activation of pro-inflammatory MPs in the chronically inflamed brain.

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Adkins, Caleb, and Michelle Chandley. "Neuroinflammation in the C1q/TNF-related over-expression mouse model of chronic ethanol exposure." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/35.

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Alcohol use can negatively impact financial, cognitive, and psychiatric aspects of human life. In the brain, alcohol can have many devastating effects. Alcohol is a well-known cytotoxic agent that can cause specific brain pathology in humans; however, the exact biological mechanisms are not well-elucidated. Animal models are invaluable tools to investigate potential novel treatments in a substance abuse model. Mice studies can be used to screen for negative outcomes prior to human trials. We hypothesize that the C1q tumor necrosis factor-related protein, CTRP3, overexpression in mice reduces neuroinflammation from ethanol consumption that has been coupled with a high fat diet when compared to control mice. The CTRP family of proteins are adipokines and CTRP3 specifically influences cell viability, metabolism, and peripheral inflammation levels. Antibody specific immunoblotting is used to probe protein expression changes in neuroinflammatory markers in mouse cerebellum brain tissue in an overexpression mouse model of CTRP3 when compared to high-fat ethanol exposed mice and baseline control mice. The two proteins examined are MAG and GFAP. Myelin associated glycoprotein, or MAG, is a protein expressed by oligodendrocytes that mediate axonal growth and myelin interactions with neurons in the brain. Oligodendrocytes are extremely sensitive to oxidative stress to which cognitive deficits in ethanol exposure is thought to be attributed. Glial fibrillary acidic protein, or GFAP, is a marker of astrocyte reactivity. Astrocytes are cells in the brain that are responsible for environmental stabilization and actively participate in neurotransmission. Currently, GFAP alterations in ethanol-exposed animals are dose and age dependent. We chose to use young adult mice where GFAP reactiveness is increased during chronic ethanol exposure. The proposed studies are essential in determining CTRP3’s relationship to detrimental neuroinflammatory effects of alcohol and high fat diet in mice. The data obtained from these studies will provide compelling evidence for future clinical trials to investigate CTRP3 as a therapeutic agent in people with a high fat diet that use alcohol chronically.

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Drieu, Antoine. "La neuroinflammation "invisible" dans les atteintes cérébrales aigue et chronique." Thesis, Normandie, 2018. http://www.theses.fr/2018NORMC422/document.

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L’inflammation est un processus essentiel à prendre en compte dans la pratique clinique. Nous avons montré durant cette thèse que le statut (neuro)inflammatoire précédant la survenue d’une pathologie cérébrale est à prendre en compte nécessairement puisqu’il modifie drastiquement la réponse inflammatoire suite à un deuxième stimulus comme la survenue d’un AVC. Il est d’autant plus important que 90% des AVC sont associés à des comorbidités comme l’hypertension artérielle, le diabète ou la consommation chronique d’alcool, qui ont d’ores et déjà été décrites comme des maladies avec une composante inflammatoire. Nous avons caractérisé ce statut neuroinflammatoire silencieux, aussi appelé priming, dans le cadre de la consommation chronique d’alcool et dans le traumatisme crânien léger. De plus, nous avons identifié les macrophages périvasculaires comme participants à l’effet aggravateur du priming inflammatoire sur les lésions ischémiques. Ils semblent alors être une cible thérapeutique de choix et feront l’objet de futures études. Il est donc nécessaire de trouver des techniques d’imagerie non invasives pour détecter le priming. L’autoradiographie ciblant le TSPO nous a permis de révéler le priming inflammatoire dans le cadre du traumatisme crânien léger. Nous proposons, au vu de nos résultats obtenus durant cette thèse, la tomographie par émission de positons pour la détection de la neuroinflammation invisible dans les atteintes cérébrales aigüe(s) et chronique(s)
Inflammation is an essential process to be considered in clinical practice. We have shown during this thesis that the (neuro)inflammatory status preceding the occurrence of a cerebral pathology must necessarily be taken into account since it drastically modifies the inflammatory response following a second stimulus such as stroke. This is even more important given that 90% of strokes are associated with comorbidities such as chronic hypertension, diabetes or chronic alcohol consumption, for which inflammation is an important pathophysiological feature. We have characterized this silent inflammatory status, also called priming, in the context of chronic alcohol consumption and in mild traumatic brain injury. We have identified perivascular macrophages (PVM) as mediators of the aggravating effect of inflammatory priming on ischemic stroke. PVM appear to be potential therapeutic targets and will be the subject of future investigations. It is therefore necessary to find non-invasive imaging techniques to detect inflammatory priming. We show that autoradiography targeting TSPO reveals the inflammatory priming provoked by a single mild traumatic brain injury. We propose, in light of the results obtained during this thesis, the positron emission tomography imaging to detect the invisible neuroinflammation in acute and chronic brain diseases

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Viar, Kenneth E. II. "Role of SARM1 in Chronic Immune-Mediated Central Nervous System Inflammation." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5819.

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SARM1 is an injury-induced nicotinamide adenine dinucleotide nucleosidase (NADase) that was previously shown to promote axonal degeneration in response to traumatic, toxic, and excitotoxic stressors. This raises the question of whether a SARM1-dependent program of axonal degeneration is central to a common pathway contributing to disease burden in neurological disorders. The degree to and mechanism by which SARM1 inactivation decreases the pathophysiology of such disorders is of interest to establish the rationale to pursue SARM1 as a therapeutic target. In this study, we compare the course and pathology of experimental autoimmune encephalomyelitis (EAE) in Sarm1-knockout (KO) mice and wild-type littermates to test the contribution of SARM1-dependent axonal degeneration specifically in the context of chronic, immune-mediated central nervous system (CNS) inflammation. The question of whether SARM1 loss in Sarm1-KO mice would inhibit, promote, or have a negligible impact on EAE-induced axonal degeneration and more broadly CNS inflammation was explored using a variety of analyses: quantification of clinical score in a chronic EAE model, CNS immune infiltrate profile, axon initial segment morphology in layer V cortical neurons, axonal transport disruption and transection in the lumbar spinal cord. Additionally, we have proposed a method for detecting SARM1 activation in situusing a novel SARM1-mCitrine bimolecular fluorescence complementation (BiFC) technique. Successful implementation of such a molecular tool would allow for a detailed, mechanistic approach to enhance our understanding of upstream intracellular signals that trigger SARM1 activation.

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Herz, Josephine [Verfasser]. "Visualization of autoimmune processes in chronic neuroinflammation by means of two-photon laser scanning microscopy / Josephine Herz." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1025086953/34.

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Hill, Jeremy David. "THE ROLE OF GPR55 IN NEURAL STEM CELL PROLIFERATION, DIFFERENTIATION, AND IMMUNE RESPONSES TO CHRONIC, SYSTEMIC INFLAMMATION." Diss., Temple University Libraries, 2018. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/527387.

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Biomedical Sciences
Ph.D.
The cannabinoid system exerts functional regulation of neural stem cell (NSC) selfrenewal, proliferation, and differentiation during both homeostatic and pathologic conditions. Recent evidence suggests that cannabinoid signaling is neuroprotective against reduction in NSC proliferation and neurogenesis caused by a multitude of conditions including injury due to HIV-1 associated neurotoxic proteins, neuroinflammation, and stroke. Yet not all effects of cannabinoids or cannabinoid-like compounds on neurogenesis can be attributed to signaling through either of the classical cannabinoid receptors CB1 or CB2. The recently de-orphaned GPR55 is targeted by numerous cannabinoid compounds suggesting GPR55 may be causing these aberrant effects. Activation of GPR55 has shown immune-modulatory effects outside the central nervous system (CNS) and anti-inflammatory actions on microglia, the resident immune cells within the CNS. New evidence has confirmed that both human and murine NSCs express functional levels of GPR55 yet the effects that GPR55 activation has on adult neurogenesis or NSC responses to inflammation has not been elucidated. In the present study we sought to determine the role GPR55 signaling has on NSC proliferation and neurogenesis as well as possible neuroprotective mechanisms within the NSC pool in response to inflammatory insult. Activation of GPR55 increased human NSC proliferation in vitro as assessed by BrdU incorporation and flow cytometry. Neuronal differentiation was also upregulated by signaling through GPR55 under homeostatic conditions in both human and murine NSC samples. Expression of NSC differentiation markers (nestin, sox2, GFAP, S100b, DCX, bIII-tubulin) in vitro was determined by immunohistochemistry, qPCR, and flow cytometry. In vivo, C57BL/6 and GPR55-/- mice were administered the GPR55 agonist O-1602 (4 μg/kg/day) directly into the left hippocampus via stainless steel cannula connected to an osmotic mini-pump for a continuous 14 days. O-1602 treatment increased hippocampal NSC proliferation, survival, and immature neuron formation as compared to vehicle treated animals. These results were determined to be dependent on GPR55 activation as GPR55-/- animals did not show any response to agonist treatment. Interestingly, GPR55-/- mice displayed significantly reduced rates of hippocampal NSC proliferation and neuroblast formation as compared to C57BL/6 animals. Chronic production of inflammatory mediators, such as IL-1b seen in neuroinflammation, to NSCs is known to reduce proliferation rates and attenuate neurogenesis both in vitro and in vivo. Addition of GPR55 agonists to IL-1b (10 ng/mL) treated human and murine NSC samples in vitro protected against reductions in neuron formation as assessed by immunohistochemistry and flow cytometry. Moreover, inflammatory cytokine receptor mRNA expression was down regulated by GPR55 activation in a neuroprotective manner. To determine inflammatory responses in vivo, we treated C57BL/6 and GPR55-/- mice with LPS (0.2 mg/kg/day) continuously for 14 days via osmotic mini-pump. Reductions in NSC survival (as determined by BrdU incorporation), immature neurons, and neuroblast formation due to LPS were attenuated by concurrent direct intrahippocampal administration of the GPR55 agonist, O-1602 (4μg/kg/day) in C57BL/6 mice but not in GPR55-/-mice. Neuroprotection by O-1602 treatment was not found to be microglia dependent as microglia activation was not altered by agonist administration. Molecular analysis of the hippocampal region showed a suppressed ability to regulate immune responses by GPR55-/- animals manifesting in a prolonged inflammatory response (IL-1b, IL-6, TNFa) after chronic, systemic inflammation as compared to C57BL/6 animals. Taken together, these results suggest a neuroprotective role of GPR55 activation on NSCs in vitro and in vivo and that GPR55 provides a novel therapeutic target against negative regulation of hippocampal neurogenesis by inflammatory insult.
Temple University--Theses

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Книги з теми "Chronic neuroinflammation"

De Logu, Francesco, Serena Boccella, Francesca Guida, and Gabriela Trevisan, eds. The Role of Neuroinflammation in Chronic Pain Development and Maintenance. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-321-6.

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Kavelaars, Annemieke, Anibal Garza Carbajal, and Cobi J. Heijnen. Regulation of Target System Sensitivity in Neuroinflammation: Role of GRK2 in Chronic Pain. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780195394399.013.0020.

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Частини книг з теми "Chronic neuroinflammation"

Walker, Douglas G. "Inflammatory Markers in Chronic Neurodegenerative Disorders with Emphasis on Alzheimer’s Disease." In Neuroinflammation, 61–90. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-473-3_2.

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Saito, Takashi. "Chronic Neuroinflammation Underlying Pathogenesis of Alzheimer’s Disease." In Chronic Inflammation, 661–71. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56068-5_50.

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Thomas, Crawford M. "Chronic neuroinflammation and waste disposal." In Sleep and Brain Injury, 116–23. London: Routledge, 2021. http://dx.doi.org/10.4324/9780429199066-9.

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Crupi, Rosalia, Marika Cordaro, and Salvatore Cuzzocrea. "Neuroinflammation and Chronic Pelvic Pain Syndrome." In Urodynamics, Neurourology and Pelvic Floor Dysfunctions, 23–46. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-56387-5_3.

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Lisak, Robert P., and Joyce A. Benjamins. "Acute, Chronic, and Nonclassical Neuroinflammation: Definitions in a Changing Scientific Environment." In Advances in Neurobiology, 1–20. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8313-7_1.

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Lin, Chih-Peng, and Dai-Hua Lu. "Role of Neuroinflammation in Opioid Tolerance: Translational Evidence from Human-to-Rodent Studies." In Advances in Pain Research: Mechanisms and Modulation of Chronic Pain, 125–39. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1756-9_11.

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Wenk, G. L., B. Hauss-Wegrzyniak, and L. B. Willard. "Pathological and Biochemical Studies of Chronic Neuroinflammation May Lead to Therapies for Alzheimer’s Disease." In Research and Perspectives in Neurosciences, 73–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59643-8_7.

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McMillin, Matthew, and Sharon DeMorrow. "Neuroinflammatory Signals during Acute and Chronic Liver Diseases." In Mechanisms of Neuroinflammation. InTech, 2017. http://dx.doi.org/10.5772/intechopen.68938.

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Schwartz, M., and K. Baruch. "Fighting Chronic Neuroinflammation by Boosting Autoimmunity." In Translational Neuroimmunology in Multiple Sclerosis, 139–48. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801914-6.00013-1.

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Y. Kuo, Grace, Fawaz Philip Tarzi, Stan Louie, and Roy A. Poblete. "Neuroinflammation in Traumatic Brain Injury." In Traumatic Brain Injury [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105178.

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Neuroinflammation following traumatic brain injury (TBI) is an important cause of secondary brain injury that perpetuates the duration and scope of disease after initial impact. This chapter discusses the pathophysiology of acute and chronic neuroinflammation, providing insight into factors that influence the acute clinical course and later functional outcomes. Secondary injury due to neuroinflammation is described by mechanisms of action such as ischemia, neuroexcitotoxicity, oxidative stress, and glymphatic and lymphatic dysfunction. Neurodegenerative sequelae of inflammation, including chronic traumatic encephalopathy, which are important to understand for clinical practice, are detailed by disease type. Prominent research topics of TBI animal models and biomarkers of traumatic neuroinflammation are outlined to provide insight into the advances in TBI research. We then discuss current clinical treatments in TBI and their implications in preventing inflammation. To complete the chapter, recent research models, novel biomarkers, and future research directions aimed at mitigating TBI will be described and will highlight novel therapeutic targets. Understanding the pathophysiology and contributors of neuroinflammation after TBI will aid in future development of prophylaxis strategies, as well as more tailored management and treatment algorithms. This topic chapter is important to both clinicians and basic and translational scientists, with the goal of improving patient outcomes in this common disease.

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Тези доповідей конференцій з теми "Chronic neuroinflammation"

Borges, Isabella Sabião, João Victor Aguiar Moreira, Eustaquio Costa Damasceno Junior, Alencar Pereira dos Santos, Gabriela Tomás Alves, Leonardo Peixoto Garcia, Maria Fernanda Prado Rosa, et al. "Chronic inflammatory demyelinating polyradiculoneuropathy induced by paclitaxel." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.413.

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Background: Peripheral neuropathies in cancer are most often due to neurotoxic chemotherapeutic agents. Approximately 30% of patients receiving neurotoxic chemotherapy (CTX) will suffer from chemotherapy-induced peripheral neuropathy (CIPN). Paclitaxel is an extremely effective chemotherapeutic agent for the treatment of breast, ovarian, and lung cancer. However, paclitaxel-induced peripheral neuropathy occurs in 59-87% of patients who receive this drug. Paclitaxel is an anti-tubulin drug that causes microtubule stabilization, resulting in distal axonal degeneration, secondary demyelination and nerve fiber loss. Case: We present a case of a 68-year-old female patient with history of breast cancer who presented sensorial ataxia and progressive muscle weakness two months after starting CTX with paclitaxel. The physical examination showed tetraparesis with proximal predominance, areflexia, severe hypopalesthesia and postural instability. Electroneuromyography showed the existence of asymmetric demyelinating polyradiculoneuropathy, with conduction block and temporal dispersion in practically all evaluated nerves. The cerebrospinal fluid confirmed the albumin-cytological dissociation. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) was confirmed and patient underwent monthly treatment with methylprednisolone with good response. Discussion: Evidences has implicated neuroinflammation in the development of PIPN. While most CTX drugs do not cross the blood-brain-barrier, they readily penetrate the blood-nerve-barrier and bind to and accumulate in dorsal root ganglia and peripheral axons. CTX can induce neuroinflammation through activation of immune and immune- like glial cells. In fact, immune cells (e.g., macrophages, lymphocytes) and glial cells (e.g., Schwann cells) in the peripheral nervous system play important role in the induction and maintenance of neuropathy. Conclusion: CIDP should be included in the spectrum of CIPN.

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Wu, X., L. Gong, and L. Zhu. "NLRP3 Deficiency Alleviates Chronic Intermittent Hypoxia-Induced Neuroinflammation and Oxidative Stress Via Parkin-Mediated Mitophagy." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2701.

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Araujo Morera, Pamela Maria, Jose Ivo Araujo Beserra-Filho, Beatriz Soares, Vitor Ponci, Maria Aparecida Oliveira, Rafael Herling Lambertucci, Nathalia Montouro Pinheiro, et al. "Effects of dehydrodieugenol on neuroinflammation and behavior changes in mice with mixed granulocytic chronic airway inflammation." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.317.

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Aytekin, Ayşegül. "Resveratrol exhibits antidepressant-like behavior in the rat chronic unpredictable mild stress model through reducing serum corticosterone, peripheral inflammation and neuroinflammation and also maintaining hippocampal BDNF levels." In 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-214.

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Звіти організацій з теми "Chronic neuroinflammation"

Li, Xiao, GX Xu, FY Ling, ZH Yin, Y. Wei,, Y. Zhao, Xn Li, WC Qi, L. Zhao, and FR Liang. The dose-effect association between electroacupuncture sessions and its effect on chronic migraine: a protocol of a meta-regression of randomized controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0085.

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Review question / Objective: We will use a meta-regression approach to verify the dose-effect relationship between the number of electroacupuncture sessions and its effects on migraine. Condition being studied: Migraine is recurrent and chronic, requiring long-term control, but the side effects caused by long-term use limit the use of pharmacotherapy, like non-steroidal anti-inflammatory drugs (NSAIDS), ergoamines and opioids. With fewer side effects and lower cost, acupuncture is becoming a more attractive option for migraine. Relevant studies have confirmed the clinical effects of electroacupuncture on migraine and its effects on intracranial blood flow velocity, functional brain imaging and neuroinflammation. However, uncertainty exists regarding the dose-effect between electroacupuncture and migraine. In recent years, inspired by the dose-effect researches in pharmacology and epidemiology, researches focusing on the dose-effect association between acupuncture and diseases has also begun to emerge. So in this protocol, we designed to use a meta-regression approach to explore the optimal electroacupuncture dose for migraine.

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