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Relevant bibliographies by topics / Astrocytes Neuroinflammation

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Academic literature on the topic 'Astrocytes Neuroinflammation'

Author: Grafiati

Published: 10 December 2022

Last updated: 31 July 2025

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Journal articles on the topic "Astrocytes Neuroinflammation"

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Michinaga, Shotaro, and Yutaka Koyama. "Pathophysiological Responses and Roles of Astrocytes in Traumatic Brain Injury." International Journal of Molecular Sciences 22, no. 12 (2021): 6418. http://dx.doi.org/10.3390/ijms22126418.

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Traumatic brain injury (TBI) is immediate damage caused by a blow to the head resulting from traffic accidents, falls, and sporting activity, which causes death or serious disabilities in survivors. TBI induces multiple secondary injuries, including neuroinflammation, disruption of the blood–brain barrier (BBB), and brain edema. Despite these emergent conditions, current therapies for TBI are limited or insufficient in some cases. Although several candidate drugs exerted beneficial effects in TBI animal models, most of them failed to show significant effects in clinical trials. Multiple studie

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Lindman, Marissa, Juan Angel, Kimberly Newman, Colm Atkins, and Brian Daniels. "Astrocytic RIPK3 confers protection against deleterious neuroinflammation during Zika virus infection." Journal of Immunology 208, no. 1_Supplement (2022): 163.27. http://dx.doi.org/10.4049/jimmunol.208.supp.163.27.

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Abstract This study aims to identify the function(s) of RIPK3 signaling in astrocytes following Zika virus infection. Previous work found that RIPK3 signaling in Zika virus-infected neurons activates inflammatory transcription factors such as NFκB and IRF1, leading to the upregulation of inflammation-associated transcripts. We were thus interested in determining the role of RIPK3 signaling in astrocytes, which are critical regulators of neuroinflammation. Using mice with an astrocyte-specific conditional Ripk3 deletion, we found that intracranial Zika virus infection was significantly more let

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Preato, André Maciel, Ester da Silva Pinheiro, Tatiana Rosado Rosenstock, and Isaias Glezer. "The Relevance of Astrocytic Cell Culture Models for Neuroinflammation in Neurodegeneration Research." Neuroglia 5, no. 1 (2024): 27–49. http://dx.doi.org/10.3390/neuroglia5010003.

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Astrocytes are the predominant glial cells that provide essential support to neurons and promote microenvironment changes in neuropathological states. Astrocyte and astrocytic-like cell culture have substantially contributed to elucidating the molecular pathways involved in key glial roles, including those relevant to neurodevelopment, brain physiology and metabolism, which are not readily accessible with traditional approaches. The in vitro methodology has also been applied to neuroinflammatory and neurodegeneration contexts, revealing cellular changes involved in brain dysfunction. Astrocyte

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Zulfiqar, Shadaan, Pretty Garg, and Katja Nieweg. "Contribution of astrocytes to metabolic dysfunction in the Alzheimer’s disease brain." Biological Chemistry 400, no. 9 (2019): 1113–27. http://dx.doi.org/10.1515/hsz-2019-0140.

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AbstractHistorically considered as accessory cells to neurons, there is an increasing interest in the role of astrocytes in normal and pathological conditions. Astrocytes are involved in neurotransmitter recycling, antioxidant supply, ion buffering and neuroinflammation, i.e. a lot of the same pathways that go astray in Alzheimer’s disease (AD). AD remains the leading cause of dementia in the elderly, one for which there is still no cure. Efforts in AD drug development have largely focused on treating neuronal pathologies that appear relatively late in the disease. The neuroenergetic hypothesi

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Karpuk, Nikolay, Maria Burkovetskaya, and Tammy Kielian. "Neuroinflammation alters voltage-dependent conductance in striatal astrocytes." Journal of Neurophysiology 108, no. 1 (2012): 112–23. http://dx.doi.org/10.1152/jn.01182.2011.

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Neuroinflammation has the capacity to alter normal central nervous system (CNS) homeostasis and function. The objective of the present study was to examine the effects of an inflammatory milieu on the electrophysiological properties of striatal astrocyte subpopulations with a mouse bacterial brain abscess model. Whole cell patch-clamp recordings were performed in striatal glial fibrillary acidic protein (GFAP)-green fluorescent protein (GFP)+ astrocytes neighboring abscesses at postinfection days 3 or 7 in adult mice. Cell input conductance ( Gi) measurements spanning a membrane potential ( Vm

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Kim, Jae-Hong, Nakamura Michiko, In-Sun Choi, et al. "Aberrant activation of hippocampal astrocytes causes neuroinflammation and cognitive decline in mice." PLOS Biology 22, no. 7 (2024): e3002687. http://dx.doi.org/10.1371/journal.pbio.3002687.

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Reactive astrocytes are associated with neuroinflammation and cognitive decline in diverse neuropathologies; however, the underlying mechanisms are unclear. We used optogenetic and chemogenetic tools to identify the crucial roles of the hippocampal CA1 astrocytes in cognitive decline. Our results showed that repeated optogenetic stimulation of the hippocampal CA1 astrocytes induced cognitive impairment in mice and decreased synaptic long-term potentiation (LTP), which was accompanied by the appearance of inflammatory astrocytes. Mechanistic studies conducted using knockout animal models and hi

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Zhang, Xiang, Hao Yao, Qingqing Qian, Nana Li, Wenjie Jin, and Yanning Qian. "Cerebral Mast Cells Participate In Postoperative Cognitive Dysfunction by Promoting Astrocyte Activation." Cellular Physiology and Biochemistry 40, no. 1-2 (2016): 104–16. http://dx.doi.org/10.1159/000452528.

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Background: Astrocytes, the major glial cell type that has been increasingly recognized as contributing to neuroinflammation, are critical in the occurrence and development of postoperative cognitive dysfunction (POCD). Although emerging evidence showed that brain mast cells (MCs) are the "first responders” in neuroinflammation, little is known about the functional communication between MCs and astrocytes. Methods: In this study, we investigated the potential regulation of astrocyte activation by MCs. Rats received an intracerebroventricular injection of Cromolyn (an MC stabilizer) or sterile

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Phillips, Emma C., Cara L. Croft, Ksenia Kurbatskaya, et al. "Astrocytes and neuroinflammation in Alzheimer's disease." Biochemical Society Transactions 42, no. 5 (2014): 1321–25. http://dx.doi.org/10.1042/bst20140155.

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Increased production of amyloid β-peptide (Aβ) and altered processing of tau in Alzheimer's disease (AD) are associated with synaptic dysfunction, neuronal death and cognitive and behavioural deficits. Neuroinflammation is also a prominent feature of AD brain and considerable evidence indicates that inflammatory events play a significant role in modulating the progression of AD. The role of microglia in AD inflammation has long been acknowledged. Substantial evidence now demonstrates that astrocyte-mediated inflammatory responses also influence pathology development, synapse health and neurode

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Jáuregui, Gretsen Velezmoro, and Vladimir Parpura. "Neuron-Astrocyte Interactions in Aging and Alzheimer's Disease: Dysregulation of Amyloid Precursor Protein." Ageing & Longevity, no. 2. 2025 (February 27, 2025): 117–28. https://doi.org/10.47855/jal9020-2025-2-3.

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Amyloid precursor protein (APP) is central to Alzheimer's disease (AD) by its role in Aβ build-up and in neuronal and astrocytic malfunction. The major risk factor for late-onset AD is aging, which increases APP processing in both neurons and astrocytes, and consequently increases Aβ production. This focused review covers the subjects of how aging and AD affect APP dynamics within the both cell types and how astrocytes dysfunction can enhance neuroinflammation and neuronal dysfunction and injury. We discuss the interplay between neurons and astrocytes in aging and AD brains, where bi-direction

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Hansson, Elisabeth. "Long-term pain, neuroinflammation and glial activation." Scandinavian Journal of Pain 1, no. 2 (2010): 67–72. http://dx.doi.org/10.1016/j.sjpain.2010.01.002.

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AbstractNociceptive and neuropathic pain signals are known to result from noxious stimuli, which are converted into electrical impulses within tissue nociceptors. There is a complex equilibrium of pain-signalling and pain-relieving pathways connecting PNS and CNS. Drugs against long-term pain are today directed against increased neuronal excitability, mostly with less success.An injury often starts with acute physiological pain, which becomes inflammatory, nociceptive, or neuropathic, and may be transferred into long-term pain. Recently a low-grade inflammation was identified in the spinal cor

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Dissertations / Theses on the topic "Astrocytes Neuroinflammation"

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Brothers, Holly M. "Neuroinflammation, Glutamate Regulation and Memory." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1363603410.

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Wu, Celina. "Dual agonist-antagonist functions of FTY720 influence neuroinflammation-relevant responses in human astrocytes." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110720.

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Astrocytes are the most abundant glia in the central nervous system (CNS), classically identified by their high expression of the intermediate filament, glial fibrillary acidic protein (GFAP). Astrocytes participate in a number of biochemical events important for CNS functions and play a dynamic role in regulating CNS injury/repair processes. In chronic inflammatory conditions such as multiple sclerosis (MS), astrocytes undergo pathophysiological changes that lead to a feature termed astrogliosis (Liberto, Albrecht et al. 2004; Sidoryk-Wegrzynowicz, Wegrzynowicz et al. 2011). Astrogliosis is c

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Hoskins, Andrew. "The Role of IRF1 in the Brain and in Adaptive Responses of Astrocytes." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5757.

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In neurodegenerative diseases, the CNS becomes inflamed through activation of pathways, including the NF-B pathway. Some of the therapies for those diseases target neuroinflammatory pathways. Here, we explore the mechanisms for the upregulation of a subset of genes following a restimulation of the NF-B pathway. We discover that this upregulation occurs independent of IRF1 expression and type 1 interferon signaling. A knockdown of IRF1 using siRNA and an inhibition of JAK proteins using inhibitor AG490 both had no effect on priming. A secreted factor was found to upregulate the expression of bo

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Clement, Tifenn. "Contribution of astrocytes in brain vulnerability after juvenile mild traumatic brain injury." Thesis, Bordeaux, 2020. http://www.theses.fr/2020BORD0141.

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Les astrocytes sont des cellules cruciales pour une variété de fonctions physiologiques cérébrales telles que l’homéostasie, le métabolisme, le couplage neurovasculaire ou la régulation de la neurotransmission. Lors de lésions cérébrales, les astrocytes deviennent réactifs et tiennent un rôle prépondérant dans la réponse neuroinflammatoire. Cette réactivité astrocytaire est hétérogène et dépend de nombreux paramètres tels que le type et la sévérité de la lésion, la proximité de l’astrocyte à la lésion, ou encore l’état de maturité du cerveau. Cependant, la réponse spécifique des astrocytes au

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Phillips, Emma Claire. "Investigating the contribution of astrocytes and neuroinflammation to pathological tau changes in Alzheimer's disease." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/investigating-the-contribution-of-astrocytes-and-neuroinflammation-to-pathological-tau-changes-in-alzheimers-disease(d96f6fa6-6870-4461-82b2-0a19d5507eab).html.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterised by accumulation of ß-amyloid in extracellular plaques, intracellular neurofibrillary tangles composed of abnormally phosphorylated and aggregated tau, and widespread synaptic dysfunction and neuron loss that underlie the clinical symptoms of AD. Glial activation and a neuroinflammatory immune response is also a key aspect of the pathological progression of AD. The activation of astrocytes appears to be particularly associated with pathological changes in tau. This thesis aims to investigate the association betwee

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Domiziana, De Tommaso. "Astrocytes contribute to neuroinflammation during EAE by shaping the CNS microenvironment via Rai signalling." Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1105117.

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Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS). One of the pathological hallmarks of MS is the T cells-mediated destruction of myelin sheath, which result in axonal damage and subsequent neurological dysfunction. Current MS therapies are focused on immunosuppression as they are aimed at limiting the entry of immune cells into CNS, thereby preventing neuroinflammation. Although these therapies have been shown to be potent disease-modifying agents they fail to prevent or reverse disease progression. Astrocytes, among CNS resident cells, has been recently sug

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Dorey, Evan J. "Apolipoprotein E Isoforms Differentially Regulate Amyloid-β Stimulated Inflammation in Rat and Mouse Astrocytes". Thesis, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23581.

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Neuroinflammation occurs in Alzheimer’s disease (AD) brain, and plays a role in neurodegeneration. The main aim of this study was to determine how treatments with exogenous apolipoprotein E (ApoE2, E3 and E4 isoforms), a genetic risk factor for AD, affects the amyloid-β (Aβ) induced inflammatory response in vitro in astrocytes. Recombinant, lipid-free ApoE4 was found not to affect Aβ-induced inflammation in rat astrocytes, while ApoE2 showed a protective effect. Mouse cells expressing human ApoE isoforms, which have similar lipidation and modification to native human ApoE, showed ApoE4 promoti

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Hsu, Meng-Ping. "Mechanisms Underlying Specificity in the Biology of the IL-6/gp130 Cytokines in Astrocytes and Microglia." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/18014.

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The gp130 family of cytokines includes IL-6, OSM, LIF, IL-11, CNTF, CLC/CLF-1 and CT-1. Members of this family are structurally similar and bind to at least one subunit of gp130 in their receptor complexes. Furthermore, they activate common signal transduction pathways, including the JAK/STAT and SHP2 pathways. However, despite these common features, cytokine-specific functions are known to exist. Two types of glial cells, astrocytes and microglia, are involved in the host response against CNS insults and release a variety of inflammatory cytokines and chemokines, including gp130 cytokines. Ho

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Ceyzériat, Kelly. "Modulation de la réactivité astrocytaire par ciblage de la voie JAK2-STAT3 : conséquences dans des modèles murins de la maladie d’Alzheimer." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS556/document.

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Les astrocytes sont des éléments clés de la physiologie cérébrale. Dans les maladies neurodégénératives comme la maladie d’Alzheimer (MA), les astrocytes deviennent réactifs. Cette réactivité astrocytaire (RA) est essentiellement caractérisée par des changements morphologiques. En revanche, les effets de la réactivité sur les fonctions de support des astrocytes sont mal connus. De plus, les cascades de signalisation qui conduisent à la RA restent à déterminer. Les objectifs de ce projet étaient de : 1/ démontrer que la voie JAK2-STAT3 (Janus Kinase 2 - Signal Transducer and Activator of Transc

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Frakes, Ashley E. "The Role of Neuroinflammation in the Pathogenesis of Amyotrophic Lateral Sclerosis." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1417649954.

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Book chapters on the topic "Astrocytes Neuroinflammation"

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Meares, Gordon P., and Etty N. Benveniste. "Inflammation and the Pathophysiology of Astrocytes in Neurodegenerative Diseases." In Neuroinflammation and Neurodegeneration. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1071-7_4.

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Tewari, Manju, and Pankaj Seth. "Astrocytes in Neuroinflammation and Neuronal Disorders: Shifting the Focus from Neurons." In Inflammation: the Common Link in Brain Pathologies. Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1711-7_3.

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Connolly, Kevin, Mikael Lehoux, Benedetta Assetta, and Yu-Wen Alvin Huang. "Modeling Cellular Crosstalk of Neuroinflammation Axis by Tri-cultures of iPSC-Derived Human Microglia, Astrocytes, and Neurons." In Stem Cell-Based Neural Model Systems for Brain Disorders. Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3287-1_7.

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Kriz, Jasna. "Neuron–Astrocyte Interactions in Neuroinflammation." In Advances in Neurobiology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8313-7_5.

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Mishra, Pooja Shree, Anu Mary Varghese, K. Vijayalakshmi, et al. "Interplay Between Microglia and Astrocytes During Neuroinflammation: Lessons Learnt from In Vitro and In Vivo Models of Sporadic Amyotrophic Lateral Sclerosis." In The Biology of Glial Cells: Recent Advances. Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8313-8_16.

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Facci, Laura, Massimo Barbierato, and Stephen D. Skaper. "Astrocyte/Microglia Cocultures as a Model to Study Neuroinflammation." In Neurotrophic Factors. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7571-6_10.

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Bir, Shyamal C., Oleg Y. Chernyshev, and Alireza Minagar. "Roles of Macrophages and Astrocytes in Pathogenesis of Multiple Sclerosis." In Neuroinflammation. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-811709-5.00028-4.

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Boulbaroud, Samira, Hanane Khalki, and Fatima Zahra Azzaoui. "Cognitive Function Involving Glial Cells." In Physiology and Function of Glial Cells in Health and Disease. IGI Global, 2023. http://dx.doi.org/10.4018/978-1-6684-9675-6.ch003.

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Astrocytes, once considered passive support cells in the central nervous system, are now recognized as dynamic contributors to neuronal processes. They play pivotal roles in regulating synaptic transmission, modulating excitability, and influencing synapse formation. These non-neuronal cells release gliotransmitters like glutamate, affecting synaptic activity. Dysfunctions in astrocytes are linked to neurodegenerative and psychiatric disorders. In neurodegenerative disorders like Alzheimer's and Parkinson's, astrocytic dysfunction plays distinct roles. While astrocytes may not significantly co

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Munir, Farwa, Nida Islam, Muhammad Hassan Nasir, et al. "Impact of Hypoxia on Astrocyte Induced Pathogenesis." In Astrocytes in Brain Communication and Disease [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106263.

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Astrocytes are the most abundant cells of the central nervous system. These cells are of diverse types based on their function and structure. Astrocyte activation is linked mainly with microbial infections, but long-term activation can lead to neurological impairment. Astrocytes play a significant role in neuro-inflammation by activating pro-inflammatory pathways. Activation of interleukins and cytokines causes neuroinflammation resulting in many neurodegenerative disorders such as stroke, growth of tumours, and Alzheimer’s. Inflammation of the brain hinders neural circulation and compromises

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Soytürk, Hayriye, Ümit Kiliç, Cansu Önal, Ayşegül Yildiz, Özge Kaya, and Ayla Gencan. "The Role and Importance of Neuroinflammation in Biopsychiatry." In Mental Health - Innovations in Therapy and Treatment [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1009524.

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Neuroinflammation is an inflammatory response that affects the central nervous system. This process involves the activation of immune cells like microglia and astrocytes, as well as the production of inflammatory chemicals like cytokines and chemokines. Neuroinflammation can be caused by a variety of circumstances, including trauma, infection, autoimmune illnesses, environmental factors, any stress scenario, and neurodegenerative diseases. Neuroinflammation is thought to be connected with a variety of psychiatric disorders. These illnesses include depression, anxiety disorders, schizophrenia,

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Conference papers on the topic "Astrocytes Neuroinflammation"

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Chen, Wenjing, Xiaotong Gu, and Feifan Zhou. "Photobiomodulation attenuates neuroinflammation in primary astrocytes identified by transcriptome analysis." In Biophotonics and Immune Responses XX, edited by Wei R. Chen and Feifan Zhou. SPIE, 2025. https://doi.org/10.1117/12.3039921.

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Zhang, Valentina. "Cross-Disease Bioinformatics Analysis to Elucidate Roles of Astrocytic Pathways Regulating Neuroinflammation in Autism Spectrum Disorder." In ICCBB 2022: 2022 6th International Conference on Computational Biology and Bioinformatics. ACM, 2022. http://dx.doi.org/10.1145/3589437.3589441.

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Zhang, Valentina. "Cross-disease Transcriptomic Analysis Elucidating the Roles of Astrocytic Signaling Pathways Regulating Neuroinflammation in Autism Spectrum Disorder (S2.003)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000202121.

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Reports on the topic "Astrocytes Neuroinflammation"

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Rumbaut Gil, Ana Laura. A Systemic Analysis of Vascular Dysfunction in Parkinson’s Disease: Reviewing the Roles of Astrocytes and COX-2. Florida International University, 2025. https://doi.org/10.25148/fiuurj.3.1.6.

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Although Parkinson’s Disease (PD) is the second most prevalent neurodegenerative disease in the U.S., the pathology remains an enigma. Many neuroinflammation hypotheses have been studied to explain its development. It’s shown that inflammatory markers such as COX-2 activity, which synthesizes the potent vasodilator PGE2, are overexpressed in PD. Additionally, astrocytes, regulators of inflammation in the brain and BBB, undergo important changes during PD. However, the vascular consequences that all this has for PD-led neurodegeneration are relatively unexplored. We conducted a systemic review

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