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Journal articles on the topic 'Astrocytes Neuroinflammation'

Author: Grafiati

Published: 10 December 2022

Last updated: 31 July 2025

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1

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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10

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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Gayen, Manoshi, Manish Bhomia, Nagaraja Balakathiresan, and Barbara Knollmann-Ritschel. "Exosomal MicroRNAs Released by Activated Astrocytes as Potential Neuroinflammatory Biomarkers." International Journal of Molecular Sciences 21, no. 7 (2020): 2312. http://dx.doi.org/10.3390/ijms21072312.

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Neuroinflammation is a hallmark of several neurodegenerative diseases and disorders, including traumatic brain injury (TBI). Neuroinflammation results in the activation of glial cells which exacerbates the neuroinflammatory process by secretion of pro-inflammatory cytokines and results in disruption of glial transmission networks. The glial cells, including astrocytes, play a critical role in the maintenance of homeostasis in the brain. Activated astrocytes release several factors as part of the inflammatory process including cytokines, proteins, and microRNAs (miRNAs). MiRNAs are noncoding RN

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He, Tingting, Guo-Yuan Yang, and Zhijun Zhang. "Crosstalk of Astrocytes and Other Cells during Ischemic Stroke." Life 12, no. 6 (2022): 910. http://dx.doi.org/10.3390/life12060910.

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Stroke is a leading cause of death and long-term disability worldwide. Astrocytes structurally compose tripartite synapses, blood–brain barrier, and the neurovascular unit and perform multiple functions through cell-to-cell signaling of neurons, glial cells, and vasculature. The crosstalk of astrocytes and other cells is complicated and incompletely understood. Here we review the role of astrocytes in response to ischemic stroke, both beneficial and detrimental, from a cell–cell interaction perspective. Reactive astrocytes provide neuroprotection through antioxidation and antiexcitatory effect

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Zhao, Yanxiang, Yingying Huang, Ying Cao, and Jing Yang. "Astrocyte-Mediated Neuroinflammation in Neurological Conditions." Biomolecules 14, no. 10 (2024): 1204. http://dx.doi.org/10.3390/biom14101204.

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Astrocytes are one of the key glial types of the central nervous system (CNS), accounting for over 20% of total glial cells in the brain. Extensive evidence has established their indispensable functions in the maintenance of CNS homeostasis, as well as their broad involvement in neurological conditions. In particular, astrocytes can participate in various neuroinflammatory processes, e.g., releasing a repertoire of cytokines and chemokines or specific neurotrophic factors, which result in both beneficial and detrimental effects. It has become increasingly clear that such astrocyte-mediated neu

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Takahashi, Shinichi, and Kyoko Mashima. "Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease." Antioxidants 11, no. 1 (2022): 170. http://dx.doi.org/10.3390/antiox11010170.

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Oxidative stress and neuroinflammation are common bases for disease onset and progression in many neurodegenerative diseases. In Parkinson disease, which is characterized by the degeneration of dopaminergic neurons resulting in dopamine depletion, the pathogenesis differs between hereditary and solitary disease forms and is often unclear. In addition to the pathogenicity of alpha-synuclein as a pathological disease marker, the involvement of dopamine itself and its interactions with glial cells (astrocyte or microglia) have attracted attention. Pacemaking activity, which is a hallmark of dopam

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Nikonenko, A. G. "Astrocytes play critical roles in neuroinflammation and Parkinson’s disease." Fiziolohichnyĭ zhurnal 70, no. 6 (2024): 110–17. https://doi.org/10.15407/fz70.06.110.

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Parkinson’s disease (PD) is a multifactorial disorder characterized mainly by the loss of dopaminergic neurons in the substantia nigra of the brain. The pathogenesis of a spontaneous PD is suggested to be multifactorial, an aberrant immune function being one of the factors influencing PD-associated neurodegeneration. It was found that negrostriatal astrocytes get involved in this process. Astrocytes play vital roles in brain homeostasis as well as participate in the local innate immune response triggered by a variety of insults. Astrocytes are not immune cells, but when sensing injury-associat

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Michinaga, Shotaro, Shigeru Hishinuma, and Yutaka Koyama. "Roles of Astrocytic Endothelin ETB Receptor in Traumatic Brain Injury." Cells 12, no. 5 (2023): 719. http://dx.doi.org/10.3390/cells12050719.

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Traumatic brain injury (TBI) is an intracranial injury caused by accidents, falls, or sports. The production of endothelins (ETs) is increased in the injured brain. ET receptors are classified into distinct types, including ETA receptor (ETA-R) and ETB receptor (ETB-R). ETB-R is highly expressed in reactive astrocytes and upregulated by TBI. Activation of astrocytic ETB-R promotes conversion to reactive astrocytes and the production of astrocyte-derived bioactive factors, including vascular permeability regulators and cytokines, which cause blood–brain barrier (BBB) disruption, brain edema, an

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Mordovina, Alina I., Ekaterina E. Rudenko, and Tatiana A. Demura. "Role of astrocytes in neuroinflammation (review)." Saratov Journal of Medical Scientific Research 19, no. 1 (2023): 89–95. http://dx.doi.org/10.15275/ssmj1901089.

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Objective: to present up-to-date scientific information concerning the role of astrocytes in neuroinflammation. A total of 63 publications were analyzed, obtained from Cochrane Library and PubMed using the following search queries: "astrocytes and neuroinflammation", "reactive astrocytes", "neuroglia and neuroinflammation". 45 publications were selected for the review. The analyzed literature was published in the year range of 2000 to 2020. It comes to a conclusion that the role of astrocytes in neuroinflammation is controversial. The cells have both protective and destructive effects. It is i

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18

Park, Gyeongah, Zhen Jin, Hui Lu, and Jianyang Du. "Clearing Amyloid-Beta by Astrocytes: The Role of Rho GTPases Signaling Pathways as Potential Therapeutic Targets." Brain Sciences 14, no. 12 (2024): 1239. https://doi.org/10.3390/brainsci14121239.

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Astrocytes, vital support cells in the central nervous system (CNS), are crucial for maintaining neuronal health. In neurodegenerative diseases such as Alzheimer’s disease (AD), astrocytes play a key role in clearing toxic amyloid-β (Aβ) peptides. Aβ, a potent neuroinflammatory trigger, stimulates astrocytes to release excessive glutamate and inflammatory factors, exacerbating neuronal dysfunction and death. Recent studies underscore the role of Rho GTPases—particularly RhoA, Rac1, and Cdc42—in regulating Aβ clearance and neuroinflammation. These key regulators of cytoskeletal dynamics and int

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Martorana, Francesca, Maria Foti, Assunta Virtuoso та ін. "Differential Modulation of NF-κB in Neurons and Astrocytes Underlies Neuroprotection and Antigliosis Activity of Natural Antioxidant Molecules". Oxidative Medicine and Cellular Longevity 2019 (14 серпня 2019): 1–16. http://dx.doi.org/10.1155/2019/8056904.

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Neuroinflammation, a hallmark of chronic neurodegenerative disorders, is characterized by sustained glial activation and the generation of an inflammatory loop, through the release of cytokines and other neurotoxic mediators that cause oxidative stress and limit functional repair of brain parenchyma. Dietary antioxidants may protect against neurodegenerative diseases by counteracting chronic neuroinflammation and reducing oxidative stress. Here, we describe the effects of a number of natural antioxidants (polyphenols, carotenoids, and thiolic molecules) in rescuing astrocytic function and neur

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Lee, Bina, Ingabire Ines, Jihyun Je, et al. "Effect of Renal Ischemia Reperfusion on Brain Neuroinflammation." Biomedicines 10, no. 11 (2022): 2993. http://dx.doi.org/10.3390/biomedicines10112993.

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Acute kidney injury (AKI) is an inflammatory sequence. It can lead to distant organ injury, including damage to the central nervous system (CNS), mediated by increased circulating cytokines and other inflammatory mediators. It can also lead to increased blood–brain barrier (BBB) permeability. However, the effect of AKI on the inflammatory response of the brain has not yet been investigated. Therefore, we observed the effect of AKI on BBB permeability, microglia and astrocyte activation, and neuronal toxicity in the brain. The striatum and ventral midbrain, known to control overall movement, se

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Perelroizen, R., B. Philosof, N. Budick-Harmelin, et al. "P12.15.B Astrocyte immunometabolic regulation of the glioblastoma microenvironment drives tumor pathogenicity." Neuro-Oncology 24, Supplement_2 (2022): ii80. http://dx.doi.org/10.1093/neuonc/noac174.280.

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Abstract Background Malignant brain tumors are the cause of a disproportionate level of morbidity and mortality among cancer patients, an unfortunate statistic that has remained constant for decades. Despite considerable advances in the molecular characterization of these tumors, targeting the cancer cells has yet to produce significant advances in treatment. An alternative strategy is to target cells in the glioblastoma microenvironment, such as tumor associated astrocytes. Astrocytes control multiple processes in health and disease, ranging from maintaining the brain's metabolic homeostasis,

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Szeky, Balazs, Veronika Jurakova, Eliska Fouskova, et al. "Efficient derivation of functional astrocytes from human induced pluripotent stem cells (hiPSCs)." PLOS ONE 19, no. 12 (2024): e0313514. https://doi.org/10.1371/journal.pone.0313514.

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Astrocytes are specialized glial cell types of the central nervous system (CNS) with remarkably high abundance, morphological and functional diversity. Astrocytes maintain neural metabolic support, synapse regulation, blood-brain barrier integrity and immunological homeostasis through intricate interactions with other cells, including neurons, microglia, pericytes and lymphocytes. Due to their extensive intercellular crosstalks, astrocytes are also implicated in the pathogenesis of CNS disorders, such as ALS (amyotrophic lateral sclerosis), Parkinson’s disease and Alzheimer’s disease. Despite

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Filippini, Alice, Valentina Salvi, Vincenzo Dattilo та ін. "LRRK2 Kinase Inhibition Attenuates Astrocytic Activation in Response to Amyloid β1-42 Fibrils". Biomolecules 13, № 2 (2023): 307. http://dx.doi.org/10.3390/biom13020307.

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Intracerebral accumulation of amyloid-β in the extracellular plaques of Alzheimer’s disease (AD) brains represents the main cause of reactive astrogliosis and neuroinflammatory response. Of relevance, leucine-rich repeat kinase 2 (LRRK2), a kinase linked to genetic and sporadic Parkinson’s disease (PD), has been identified as a positive mediator of neuroinflammation upon different inflammatory stimuli, however its pathogenicity in AD remains mainly unexplored. In this study, by using pharmacological inhibition of LRRK2 and murine primary astrocytes, we explored whether LRRK2 regulates astrocyt

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Chen, Kun, Haoyang Wang, Iqra Ilyas, Arif Mahmood, and Lijun Hou. "Microglia and Astrocytes Dysfunction and Key Neuroinflammation-Based Biomarkers in Parkinson’s Disease." Brain Sciences 13, no. 4 (2023): 634. http://dx.doi.org/10.3390/brainsci13040634.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease, with symptoms such as tremor, bradykinesia with rigidity, and depression appearing in the late stage of life. The key hallmark of PD is the loss or death of dopaminergic neurons in the region substantia nigra pars compacta. Neuroinflammation plays a key role in the etiology of PD, and the contribution of immunity-related events spurred the researchers to identify anti-inflammatory agents for the treatment of PD. Neuroinflammation-based biomarkers have been identified for diagnosing PD, and many cellular and animal mo

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Provenzano, Francesca, Carola Torazza, Tiziana Bonifacino, Giambattista Bonanno, and Marco Milanese. "The Key Role of Astrocytes in Amyotrophic Lateral Sclerosis and Their Commitment to Glutamate Excitotoxicity." International Journal of Molecular Sciences 24, no. 20 (2023): 15430. http://dx.doi.org/10.3390/ijms242015430.

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In the last two decades, there has been increasing evidence supporting non-neuronal cells as active contributors to neurodegenerative disorders. Among glial cells, astrocytes play a pivotal role in driving amyotrophic lateral sclerosis (ALS) progression, leading the scientific community to focus on the “astrocytic signature” in ALS. Here, we summarized the main pathological mechanisms characterizing astrocyte contribution to MN damage and ALS progression, such as neuroinflammation, mitochondrial dysfunction, oxidative stress, energy metabolism impairment, miRNAs and extracellular vesicles cont

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Seth, Ratanesh K., Dipro Bose, Punnag Saha, et al. "Altered Gut DNA virome diversity associated HMGB1 release regulates reactive Astrocytes-induced IL6 release preferably via TLR4-NFkB pathway in experimental Gulf War Illness." Journal of Immunology 204, no. 1_Supplement (2020): 64.15. http://dx.doi.org/10.4049/jimmunol.204.supp.64.15.

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Abstract In a recent study, we showed that the gut DNA bacteriophage dysbiosis in Gulf War Illness (GWI) was strongly associated with compromised intestinal epithelial cell integrity, increased circulatory IL6 and neuroinflammation. The current study further investigates the mechanism of DNA bacteriophage-IL6 axis in neuroinflammation. Advancing the previous findings, we show that viral dysbiosis positively correlated with high mobility group box protein 1 (HMGB1; a damage-associated molecular pattern) expression and release in circulation following GWI induction in mice. The circulatory HMGB1

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Frost, Georgia R., and Yue-Ming Li. "The role of astrocytes in amyloid production and Alzheimer's disease." Open Biology 7, no. 12 (2017): 170228. http://dx.doi.org/10.1098/rsob.170228.

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Alzheimer's disease (AD) is marked by the presence of extracellular amyloid beta (Aβ) plaques, intracellular neurofibrillary tangles (NFTs) and gliosis, activated glial cells, in the brain. It is thought that Aβ plaques trigger NFT formation, neuronal cell death, neuroinflammation and gliosis and, ultimately, cognitive impairment. There are increased numbers of reactive astrocytes in AD, which surround amyloid plaques and secrete proinflammatory factors and can phagocytize and break down Aβ. It was thought that neuronal cells were the major source of Aβ. However, mounting evidence suggests tha

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Clarke, Laura E., Shane A. Liddelow, Chandrani Chakraborty, Alexandra E. Münch, Myriam Heiman, and Ben A. Barres. "Normal aging induces A1-like astrocyte reactivity." Proceedings of the National Academy of Sciences 115, no. 8 (2018): E1896—E1905. http://dx.doi.org/10.1073/pnas.1800165115.

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The decline of cognitive function occurs with aging, but the mechanisms responsible are unknown. Astrocytes instruct the formation, maturation, and elimination of synapses, and impairment of these functions has been implicated in many diseases. These findings raise the question of whether astrocyte dysfunction could contribute to cognitive decline in aging. We used the Bac-Trap method to perform RNA sequencing of astrocytes from different brain regions across the lifespan of the mouse. We found that astrocytes have region-specific transcriptional identities that change with age in a region-dep

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Puentes-Orozco, Melissa, Sonia L. Albarracin, and María Marcela Velásquez. "Neuroinflammation and major depressive disorder: astrocytes at the crossroads." Frontiers in Cellular Neuroscience 18 (November 22, 2024). http://dx.doi.org/10.3389/fncel.2024.1504555.

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Major depressive disorder is a complex and multifactorial condition, increasingly linked to neuroinflammation and astrocytic dysfunction. Astrocytes, along with other glial cells, beyond their classic functions in maintaining brain homeostasis, play a crucial role in regulating neuroinflammation and neuroplasticity, key processes in the pathophysiology of depression. This mini-review explores the involvement of astrocytes in depression emphasizing their mediation in neuroinflammation processes, the impact of astrocytic dysfunction on neuroplasticity, and the effect of some antidepressants on a

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Mockenhaupt, Karli, Masoumeh Zarei‐Kheirabadi, Alexandra K. Gonsiewski, et al. "Defective Astrocyte Maturation Drives Cerebellar Neuroinflammation and Degeneration." FASEB Journal 39, no. 14 (2025). https://doi.org/10.1096/fj.202501225rr.

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ABSTRACTWhile persistent neuroinflammation and neurodegeneration are hallmarks of many diseases, the exact mechanisms triggering neurodegeneration are not fully established. Neurodegeneration is accompanied by activation of astrocytes that can have both neuroprotective and neurotoxic functions. Much less is known about how intrinsic dysfunction of astrocytes can lead to neuroinflammation and neurodegeneration. To study astrocyte‐driven neurodegeneration, we examined aging cerebella of adult astrocyte‐specific Yin Yang1 (Yy1) conditional knockout mice that contain improperly matured dysfunction

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Zimmer, Till S., Daniel Barnett, Adam L. Orr, and Anna G. Orr. "Astrocytic induction of triglyceride lipolysis in AD‐associated pathology and neuroinflammation." Alzheimer's & Dementia 20, S1 (2024). https://doi.org/10.1002/alz.093056.

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AbstractBackgroundMultiple AD risk genes are implicated in lipid metabolism, and plasma and brain lipid levels are altered in AD. Astrocytes are enriched in key lipid‐related factors and are likely contributors to altered lipid homeostasis in AD. We hypothesize that APP/Aβ‐related pathology and neuroimmune factors modulate astrocytic gene transcription that promote maladaptive changes in lipid pathways, including aberrant astrocytic production and release of lipids that could affect Aβ pathology and neuronal deficits.MethodTo investigate the effects of APP/Aβ and neuroinflammation on astrocyti

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Wang, Ting, Akira Sobue, Seiji Watanabe, et al. "Dimethyl fumarate improves cognitive impairment and neuroinflammation in mice with Alzheimer’s disease." Journal of Neuroinflammation 21, no. 1 (2024). http://dx.doi.org/10.1186/s12974-024-03046-2.

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Abstract Background Neuroinflammation substantially contributes to the pathology of Alzheimer’s disease (AD), the most common form of dementia. Studies have reported that nuclear factor erythroid 2-related factor 2 (Nrf2) attenuates neuroinflammation in the mouse models of neurodegenerative diseases, however, the detailed mechanism remains unclear. Methods The effects of dimethyl fumarate (DMF), a clinically used drug to activate the Nrf2 pathway, on neuroinflammation were analyzed in primary astrocytes and AppNL−G−F (App-KI) mice. The cognitive function and behavior of DMF-administrated App-K

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"P2Y1R silencing in Astrocytes Protected Neuroinflammation and Cognitive Decline in a Mouse Model of Alzheimer's Disease." aging and disease, 2023. http://dx.doi.org/10.14336/ad.2023.1006.

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Astrocytes, the major non-dividing glial cells in the central nervous system, exhibit hyperactivation in Alzheimer’s disease (AD), leading to neuroinflammation and cognitive impairments. P2Y1-receptor (P2Y1R) in AD brain has been pointed out some contribution to AD pathogenesis, therefore, this study aims to elucidate how astrocytic P2Y1R affects the progression of AD and explore its potential as a new target for AD therapy. In this study, we performed the two-steps verification to assess P2Y1R inhibition in AD progression: P2Y1R-KO AD mice and AD mice treated with astrocyte-specific P2Y1R gen

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Liu, Min‐Hui, Yu‐Ge Xu, Xiao‐Ni Bai, et al. "Efficient Dlx2‐mediated astrocyte‐to‐neuron conversion and inhibition of neuroinflammation by NeuroD1." Developmental Neurobiology, July 21, 2024. http://dx.doi.org/10.1002/dneu.22951.

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AbstractIn vivo astrocyte‐to‐neuron (AtN) conversion induced by overexpression of neural transcriptional factors has great potential for neural regeneration and repair. Here, we demonstrate that a single neural transcriptional factor, Dlx2, converts mouse striatal astrocytes into neurons in a dose‐dependent manner. Lineage‐tracing studies in Aldh1l1‐CreERT2 mice confirm that Dlx2 can convert striatal astrocytes into DARPP32+ and Ctip2+ medium spiny neurons (MSNs). Time‐course studies reveal a gradual conversion from astrocytes to neurons in 1 month, with a distinct intermediate state in betwee

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Guo, Qilin, Davide Gobbo, Na Zhao, et al. "Adenosine triggers early astrocyte reactivity that provokes microglial responses and drives the pathogenesis of sepsis-associated encephalopathy in mice." Nature Communications 15, no. 1 (2024). http://dx.doi.org/10.1038/s41467-024-50466-y.

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AbstractMolecular pathways mediating systemic inflammation entering the brain parenchyma to induce sepsis-associated encephalopathy (SAE) remain elusive. Here, we report that in mice during the first 6 hours of peripheral lipopolysaccharide (LPS)-evoked systemic inflammation (6 hpi), the plasma level of adenosine quickly increased and enhanced the tone of central extracellular adenosine which then provoked neuroinflammation by triggering early astrocyte reactivity. Specific ablation of astrocytic Gi protein-coupled A1 adenosine receptors (A1ARs) prevented this early reactivity and reduced the

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Nakano-Kobayashi, Akiko, Andres Canela, Toru Yoshihara, and Masatoshi Hagiwara. "Astrocyte-targeting therapy rescues cognitive impairment caused by neuroinflammation via the Nrf2 pathway." Proceedings of the National Academy of Sciences 120, no. 33 (2023). http://dx.doi.org/10.1073/pnas.2303809120.

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Neuroinflammation is a common feature of neurodegenerative disorders such as Alzheimer’s disease (AD). Neuroinflammation is induced by dysregulated glial activation, and astrocytes, the most abundant glial cells, become reactive upon neuroinflammatory cytokines released from microglia and actively contribute to neuronal loss. Therefore, blocking reactive astrocyte functions is a viable strategy to manage neurodegenerative disorders. However, factors or therapeutics directly regulating astrocyte subtypes remain unexplored. Here, we identified transcription factor NF-E2-related factor 2 (Nrf2) a

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Vidal Escobedo, Ana Abril, Facundo Peralta, Gustavo Ramón Morel, et al. "GDNF overexpression in astrocytes enhances branching and partially preserves hippocampal function in an Alzheimer’s rat model." Scientific Reports 15, no. 1 (2025). https://doi.org/10.1038/s41598-025-02881-4.

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Abstract Astrocytes are essential for maintaining neuronal health and regulating the brain’s inflammatory environment. In this study, we developed an adeno-associated viral vector (AAV9) designed to selectively overexpress glial cell line-derived neurotrophic factor (GDNF) in astrocytes, using the astrocyte-specific GFAP promoter and TdTomato for transduction tracking. This approach yielded targeted GDNF expression in hippocampal astrocytes. Sholl analysis revealed that GDNF overexpression significantly enhanced astrocytic branching complexity and process length. Using the intracerebroventricu

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Tan, Qianqian, Chenxi Zhang, Xiuqin Rao, et al. "The interaction of lipocalin-2 and astrocytes in neuroinflammation: mechanisms and therapeutic application." Frontiers in Immunology 15 (March 12, 2024). http://dx.doi.org/10.3389/fimmu.2024.1358719.

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Neuroinflammation is a common pathological process in various neurological disorders, including stroke, Alzheimer’s disease, Parkinson’s disease, and others. It involves the activation of glial cells, particularly astrocytes, and the release of inflammatory mediators. Lipocalin-2 (Lcn-2) is a secretory protein mainly secreted by activated astrocytes, which can affect neuroinflammation through various pathways. It can also act as a pro-inflammatory factor by modulating astrocyte activation and polarization through different signaling pathways, such as NF-κB, and JAK-STAT, amplifying the inflamm

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Zhou, Hang, Libin Hu, Jianru Li, et al. "AXL kinase-mediated astrocytic phagocytosis modulates outcomes of traumatic brain injury." Journal of Neuroinflammation 18, no. 1 (2021). http://dx.doi.org/10.1186/s12974-021-02201-3.

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Abstract Background Complex changes in the brain microenvironment following traumatic brain injury (TBI) can cause neurological impairments for which there are few efficacious therapeutic interventions. The reactivity of astrocytes is one of the keys to microenvironmental changes, such as neuroinflammation, but its role and the molecular mechanisms that underpin it remain unclear. Methods Male C57BL/6J mice were subjected to the controlled cortical impact (CCI) to develop a TBI model. The specific ligand of AXL receptor tyrosine kinase (AXL), recombinant mouse growth arrest-specific 6 (rmGas6)

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Gurram, Prasada Chowdari, Suman Manandhar, Sairaj Satarker, Jayesh Mudgal, Devinder Arora, and Madhavan Nampoothiri. "Dopaminergic Signaling as a Plausible Modulator of Astrocytic Toll-Like Receptor 4: A Crosstalk Between Neuroinflammation and Cognition." CNS & Neurological Disorders - Drug Targets 21 (April 13, 2022). http://dx.doi.org/10.2174/1871527321666220413090541.

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Abstract: Neuroinflammation is one of the major pathological factors leading to Alzheimer's disease (AD). The role of microglial cells in neuroinflammation associated with AD has been known since a long time. Recently, astrocytic inflammatory responses have been linked to the neuronal degeneration and pathological development of AD. Lipopolysaccharide (LPS) and Amyloid Beta (Aβ) activate astrocytes and microglial cells via toll-like 4 (TLR4) receptors leading to neuroinflammation. Reactive (activated) astrocytes mainly comprising of A1 astrocytes (A1s) are involved in neuroinflammation, and A2

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Leandrou, Emmanouela, Ioanna Chalatsa, Dimitrios Anagnostou та ін. "α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Cav3.2 calcium signaling in astrocytes". Translational Neurodegeneration 13, № 1 (2024). http://dx.doi.org/10.1186/s40035-024-00401-4.

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Abstract Background It is now realized that Parkinson’s disease (PD) pathology extends beyond the substantia nigra, affecting both central and peripheral nervous systems, and exhibits a variety of non-motor symptoms often preceding motor features. Neuroinflammation induced by activated microglia and astrocytes is thought to underlie these manifestations. α-Synuclein aggregation has been linked with sustained neuroinflammation in PD, aggravating neuronal degeneration; however, there is still a lack of critical information about the structural identity of the α-synuclein conformers that activate

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Mi, Yashi, Guoyuan Qi, Francesca Vitali, et al. "Loss of Fatty Acid Degradation by Astrocytic Mitochondria as a Mechanism of Neuroinflammation and Neurodegeneration." Alzheimer's & Dementia 19, S13 (2023). http://dx.doi.org/10.1002/alz.076572.

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AbstractBackgroundAstrocytes provide key neuronal support, and their phenotypic transformation is strongly implicated in neurodegenerative disorders including Alzheimer’s disease (AD). Metabolically, astrocytes possess modest mitochondrial oxidative phosphorylation (OxPhos) activity, yet the pathological role of astrocytic OxPhos in neurodegeneration remains to be defined.MethodWe generated the TfamAKO mice, in which the transcription factor A mitochondrial (Tfam) is deleted selectively in astrocytes. Behavioral, electrophysiological, immunostaining, transcriptomics, metabolomics, and magnetic

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Cho, Juyeong, Eun‐Bin Hong, Young‐Sik Kim, et al. "Baicalin and baicalein from Scutellaria baicalensis Georgi alleviate aberrant neuronal suppression mediated by GABA from reactive astrocytes." CNS Neuroscience & Therapeutics 30, no. 5 (2024). http://dx.doi.org/10.1111/cns.14740.

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AbstractAimsγ‐aminobutyric acid (GABA) from reactive astrocytes is critical for the dysregulation of neuronal activity in various neuroinflammatory conditions. While Scutellaria baicalensis Georgi (S. baicalensis) is known for its efficacy in addressing neurological symptoms, its potential to reduce GABA synthesis in reactive astrocytes and the associated neuronal suppression remains unclear. This study focuses on the inhibitory action of monoamine oxidase B (MAO‐B), the key enzyme for astrocytic GABA synthesis.MethodsUsing a lipopolysaccharide (LPS)‐induced neuroinflammation mouse model, we c

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Yin, Shu, Xin-yue Ma, Ying-feng Sun, et al. "RGS5 augments astrocyte activation and facilitates neuroinflammation via TNF signaling." Journal of Neuroinflammation 20, no. 1 (2023). http://dx.doi.org/10.1186/s12974-023-02884-w.

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AbstractAstrocytes contribute to chronic neuroinflammation in a variety of neurodegenerative diseases, including Parkinson's disease (PD), the most common movement disorder. However, the precise role of astrocytes in neuroinflammation remains incompletely understood. Herein, we show that regulator of G-protein signaling 5 (RGS5) promotes neurodegenerative process through augmenting astrocytic tumor necrosis factor receptor (TNFR) signaling. We found that selective ablation of Rgs5 in astrocytes caused an inhibition in the production of cytokines resulting in mitigated neuroinflammatory respons

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Lawrence, Jill M., Kayla Schardien, Brian Wigdahl, and Michael R. Nonnemacher. "Roles of neuropathology-associated reactive astrocytes: a systematic review." Acta Neuropathologica Communications 11, no. 1 (2023). http://dx.doi.org/10.1186/s40478-023-01526-9.

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AbstractIn the contexts of aging, injury, or neuroinflammation, activated microglia signaling with TNF-α, IL-1α, and C1q induces a neurotoxic astrocytic phenotype, classified as A1, A1-like, or neuroinflammatory reactive astrocytes. In contrast to typical astrocytes, which promote neuronal survival, support synapses, and maintain blood–brain barrier integrity, these reactive astrocytes downregulate supportive functions and begin to secrete neurotoxic factors, complement components like C3, and chemokines like CXCL10, which may facilitate recruitment of immune cells across the BBB into the CNS.

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Singhal, Gaurav, Saurabh Singhal, and Bernhard T. Baune. "Role of astrocyte in neuroinflammation‐induced loss in neuroplasticity and subsequent onset of depression: A systematic review." Neuroprotection, June 6, 2025. https://doi.org/10.1002/nep3.70009.

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AbstractMajor depressive disorder (MDD) is a complex psychiatric condition increasingly linked to chronic neuroinflammation, particularly in the context of aging, stress, and systemic comorbidities. While microglia have traditionally been the focus of neuroimmune studies, growing evidence highlights astrocytes as central regulators in the pathogenesis of MDD. This review synthesizes current findings on the multifaceted roles of astrocytes in neuroplasticity, neurotransmission, metabolic support, and blood‐brain barrier regulation. It explores how astrocyte reactivity and the release of pro‐inf

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Lindman, Marissa, Irving Estevez, Eduard Marmut, et al. "Astrocytic RIPK3 exerts protective anti-inflammatory activity in mice with viral encephalitis by transcriptional induction of serpins." Science Signaling 18, no. 895 (2025). https://doi.org/10.1126/scisignal.adq6422.

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Flaviviruses pose a substantial threat to public health because of their ability to infect the central nervous system (CNS). Receptor-interacting protein kinase 3 (RIPK3) is a central coordinator that promotes neuroinflammation during viral infection of the CNS, a role that occurs independently of its canonical function in inducing necroptosis. Here, we used mouse genetic tools to induce astrocyte-specific deletion, overexpression, and chemogenetic activation of RIPK3 to demonstrate an anti-inflammatory function for astrocytic RIPK3. RIPK3 activation in astrocytes promoted host survival during

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Mann, Carolyn N., Shamulailatpam Shreedarshanee Devi, Corey T. Kersting та ін. "Astrocytic α2-Na ⁺ /K ⁺ ATPase inhibition suppresses astrocyte reactivity and reduces neurodegeneration in a tauopathy mouse model". Science Translational Medicine 14, № 632 (2022). http://dx.doi.org/10.1126/scitranslmed.abm4107.

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Alzheimer’s disease (AD) is the most dominant form of dementia characterized by the deposition of extracellular amyloid plaques and intracellular neurofibrillary tau tangles (NFTs). In addition to these pathologies, an emerging pathophysiological mechanism that influences AD is neuroinflammation. Astrocytes are a vital type of glial cell that contribute to neuroinflammation, and reactive astrocytes, or astrogliosis, are a well-known pathological feature of AD. However, the mechanisms by which astrocytes contribute to the neurodegenerative process in AD have not been fully elucidated. Here, we

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Boulton, Matthew, and Ali Al-Rubaie. "Neuroinflammation and neurodegeneration following traumatic brain injuries." Anatomical Science International, May 13, 2024. http://dx.doi.org/10.1007/s12565-024-00778-2.

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AbstractTraumatic brain injuries (TBI) commonly occur following head trauma. TBI may result in short- and long-term complications which may lead to neurodegenerative consequences, including cognitive impairment post-TBI. When investigating the neurodegeneration following TBI, studies have highlighted the role reactive astrocytes have in the neuroinflammation and degeneration process. This review showcases a variety of markers that show reactive astrocyte presence under pathological conditions, including glial fibrillary acidic protein (GFAP), Crystallin Alpha-B (CRYA-B), Complement Component 3

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Zhao, Chenhui, Wei Qi, Xiaoping Lv, Xueli Gao, Chaonan Liu, and Shimin Zheng. "Elucidating the Role of Trem2 in Lipid Metabolism and Neuroinflammation." CNS Neuroscience & Therapeutics 31, no. 4 (2025). https://doi.org/10.1111/cns.70338.

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ABSTRACTBackgroundAlzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive impairment and neuroinflammation. Astrocytes play a key role in the neuroinflammatory environment of AD, especially through lipid metabolism regulation. However, the mechanisms by which astrocytes, particularly through the triggering receptor expressed on myeloid cells 2 (Trem2) receptor, contribute to lipid dysregulation and neuroinflammation in AD remain inadequately understood.MethodsWe employed an AD mouse model and integrated single‐cell RNA sequencing (scRNA‐seq), transcriptomics, and hi

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