Relevant bibliographies by topics / Astrocytes

Academic literature on the topic 'Astrocytes'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 July 2024

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Journal articles on the topic "Astrocytes"

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Nett, Wolfgang J., Scott H. Oloff, and Ken D. McCarthy. "Hippocampal Astrocytes In Situ Exhibit Calcium Oscillations That Occur Independent of Neuronal Activity." Journal of Neurophysiology 87, no. 1 (January 1, 2002): 528–37. http://dx.doi.org/10.1152/jn.00268.2001.

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Results presented in this study indicate that a large subpopulation (∼65%) of hippocampal astrocytes in situ exhibit calcium oscillations in the absence of neuronal activity. Further, the spontaneous oscillations observed within individual hippocampal astrocytes generally developed asynchronously throughout the astrocyte's fine processes and occasionally spread through a portion of that astrocyte as a calcium wave but do not appear to spread among astrocytes as an intercellular calcium wave. Bath application of cyclopiazonic acid and injection of individual astrocytes with heparin blocked astrocytic calcium oscillations. Application of tetrodotoxin or incubation of slices with bafilomycin A1 had no effect on astrocytic calcium oscillations but did block evoked and spontaneous postsynaptic currents measured in CA1 pyramidal neurons. Application of a cocktail of antagonists for metabotropic glutamate receptors and purinergic receptors had no effect on the astrocytic calcium oscillations but blocked the ability of purinergic and metabotropic glutamatergic agonists to increase astrocytic calcium levels. These results indicate that the spontaneous calcium oscillations observed in hippocampal astrocytes in situ are mediated by IP3 receptor activation, are not dependent on neuronal activity, and do not depend on activation of metabotropic glutamate receptors or purinergic receptors. To our knowledge, this is the first demonstration that astrocytes in situ exhibit intrinsic signaling. This finding supports the hypothesis that astrocytes, independent of neuronal input, may act as pacemakers to modulate neuronal activity in situ.
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Huang, Mi, Yixing Du, Conrad Kiyoshi, Xiao Wu, Candice Askwith, Dana McTigue, and Min Zhou. "Syncytial Isopotentiality: An Electrical Feature of Spinal Cord Astrocyte Networks." Neuroglia 1, no. 1 (August 24, 2018): 271–79. http://dx.doi.org/10.3390/neuroglia1010018.

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Due to strong electrical coupling, syncytial isopotentiality emerges as a physiological mechanism that coordinates astrocytes into a highly efficient system in brain homeostasis. Although this electrophysiological phenomenon has now been observed in astrocyte networks established by different astrocyte subtypes, the spinal cord remains a brain region that is still unexplored. In ALDH1L1-eGFP transgenic mice, astrocytes can be visualized by confocal microscopy and the spinal cord astrocytes in grey matter are organized in a distinctive pattern. Namely, each astrocyte resides with more directly coupled neighbors at shorter interastrocytic distances compared to protoplasmic astrocytes in the hippocampal CA1 region. In whole-cell patch clamp recording, the spinal cord grey matter astrocytes exhibit passive K+ conductance and a highly hyperpolarized membrane potential of −80 mV. To answer whether syncytial isopotentiality is a shared feature of astrocyte networks in the spinal cord, the K+ content in a physiological recording solution was substituted by equimolar Na+ for whole-cell recording in spinal cord slices. In uncoupled single astrocytes, this substitution of endogenous K+ with Na+ is known to depolarize astrocytes to around 0 mV as predicted by Goldman–Hodgkin–Katz (GHK) equation. In contrast, the existence of syncytial isopotentiality is indicated by a disobedience of the GHK predication as the recorded astrocyte’s membrane potential remains at a quasi-physiological level that is comparable to its neighbors due to strong electrical coupling. We showed that the strength of syncytial isopotentiality in spinal cord grey matter is significantly stronger than that of astrocyte network in the hippocampal CA1 region. Thus, this study corroborates the notion that syncytial isopotentiality most likely represents a system-wide electrical feature of astrocytic networks throughout the brain.
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Domingos, Cátia, Franziska E. Müller, Stefan Passlick, Dagmar Wachten, Evgeni Ponimaskin, Martin K. Schwarz, Susanne Schoch, André Zeug, and Christian Henneberger. "Induced Remodelling of Astrocytes In Vitro and In Vivo by Manipulation of Astrocytic RhoA Activity." Cells 12, no. 2 (January 15, 2023): 331. http://dx.doi.org/10.3390/cells12020331.

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Structural changes of astrocytes and their perisynaptic processes occur in response to various physiological and pathophysiological stimuli. They are thought to profoundly affect synaptic signalling and neuron-astrocyte communication. Understanding the causal relationship between astrocyte morphology changes and their functional consequences requires experimental tools to selectively manipulate astrocyte morphology. Previous studies indicate that RhoA-related signalling can play a major role in controlling astrocyte morphology, but the direct effect of increased RhoA activity has not been documented in vitro and in vivo. Therefore, we established a viral approach to manipulate astrocytic RhoA activity. We tested if and how overexpression of wild-type RhoA, of a constitutively active RhoA mutant (RhoA-CA), and of a dominant-negative RhoA variant changes the morphology of cultured astrocytes. We found that astrocytic expression of RhoA-CA induced robust cytoskeletal changes and a withdrawal of processes in cultured astrocytes. In contrast, overexpression of other RhoA variants led to more variable changes of astrocyte morphology. These induced morphology changes were reproduced in astrocytes of the hippocampus in vivo. Importantly, astrocytic overexpression of RhoA-CA did not alter the branching pattern of larger GFAP-positive processes of astrocytes. This indicates that a prolonged increase of astrocytic RhoA activity leads to a distinct morphological phenotype in vitro and in vivo, which is characterized by an isolated reduction of fine peripheral astrocyte processes in vivo. At the same time, we identified a promising experimental approach for investigating the functional consequences of astrocyte morphology changes.
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Amuti, T., I. Ouko, S. Mukonjia, I. Cheruiyot, J. Munguti, P. Mwachaka, and A. Malek. "Role of heterogeneous astrocyte receptor expression in determining astrocytic response to neuronal disorders." Anatomy Journal of Africa 7, no. 1 (April 11, 2018): 1169–74. http://dx.doi.org/10.4314/aja.v7i1.169490.

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Following neuronal disorders, astrocytes carry out either neuroprotection or neurodegeneration. Previous authors suggest that favoring of neurodegeneration or neuroprotection by astrocytes can be due to many factors such as the influence of cytokines following their binding on their receptors on astrocytes. These receptors have however been shown to be region specific and heterogeneous. Further, research exploiting their role and influence in determining astrocytic response remains partly elucidated. A review of previous and ongoing research on these receptors would be helpful in the disclosure of astrocytic responses to neuronal disorders.Keywords: Astrogliosis, Heterogenous astrocyte expression, Antagonistic astrocyte reaction, Nervous injury, Astrocyte mediated neurodegeneration
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Wolfes, Anne C., Saheeb Ahmed, Ankit Awasthi, Markus A. Stahlberg, Ashish Rajput, Daniel S. Magruder, Stefan Bonn, and Camin Dean. "A novel method for culturing stellate astrocytes reveals spatially distinct Ca2+ signaling and vesicle recycling in astrocytic processes." Journal of General Physiology 149, no. 1 (December 1, 2016): 149–70. http://dx.doi.org/10.1085/jgp.201611607.

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Interactions between astrocytes and neurons rely on the release and uptake of glial and neuronal molecules. But whether astrocytic vesicles exist and exocytose in a regulated or constitutive fashion is under debate. The majority of studies have relied on indirect methods or on astrocyte cultures that do not resemble stellate astrocytes found in vivo. Here, to investigate vesicle-associated proteins and exocytosis in stellate astrocytes specifically, we developed a simple, fast, and economical method for growing stellate astrocyte monocultures. This method is superior to other monocultures in terms of astrocyte morphology, mRNA expression profile, protein expression of cell maturity markers, and Ca2+ fluctuations: In astrocytes transduced with GFAP promoter–driven Lck-GCaMP3, spontaneous Ca2+ events in distinct domains (somata, branchlets, and microdomains) are similar to those in astrocytes co-cultured with other glia and neurons but unlike Ca2+ events in astrocytes prepared using the McCarthy and de Vellis (MD) method and immunopanned (IP) astrocytes. We identify two distinct populations of constitutively recycling vesicles (harboring either VAMP2 or SYT7) specifically in branchlets of cultured stellate astrocytes. SYT7 is developmentally regulated in these astrocytes, and we observe significantly fewer synapses in wild-type mouse neurons grown on Syt7−/− astrocytes. SYT7 may thus be involved in trafficking or releasing synaptogenic factors. In summary, our novel method yields stellate astrocyte monocultures that can be used to study Ca2+ signaling and vesicle recycling and dynamics in astrocytic processes.
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Escalada, Paula, Amaia Ezkurdia, María Javier Ramírez, and Maite Solas. "Essential Role of Astrocytes in Learning and Memory." International Journal of Molecular Sciences 25, no. 3 (February 5, 2024): 1899. http://dx.doi.org/10.3390/ijms25031899.

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One of the most biologically relevant functions of astrocytes within the CNS is the regulation of synaptic transmission, i.e., the physiological basis for information transmission between neurons. Changes in the strength of synaptic connections are indeed thought to be the cellular basis of learning and memory. Importantly, astrocytes have been demonstrated to tightly regulate these processes via the release of several gliotransmitters linked to astrocytic calcium activity as well as astrocyte–neuron metabolic coupling. Therefore, astrocytes seem to be integrators of and actors upon learning- and memory-relevant information. In this review, we focus on the role of astrocytes in learning and memory processes. We delineate the recognized inputs and outputs of astrocytes and explore the influence of manipulating astrocytes on behaviour across diverse learning paradigms. We conclude that astrocytes influence learning and memory in various manners. Appropriate astrocytic Ca2+ dynamics are being increasingly identified as central contributors to memory formation and retrieval. In addition, astrocytes regulate brain rhythms essential for cognition, and astrocyte–neuron metabolic cooperation is required for memory consolidation.
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Nassar, Ajmal, Triveni Kodi, Sairaj Satarker, Prasada Chowdari Gurram, Dinesh Upadhya, Fayaz SM, Jayesh Mudgal, and Madhavan Nampoothiri. "Astrocytic MicroRNAs and Transcription Factors in Alzheimer’s Disease and Therapeutic Interventions." Cells 11, no. 24 (December 17, 2022): 4111. http://dx.doi.org/10.3390/cells11244111.

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Astrocytes are important for maintaining cholesterol metabolism, glutamate uptake, and neurotransmission. Indeed, inflammatory processes and neurodegeneration contribute to the altered morphology, gene expression, and function of astrocytes. Astrocytes, in collaboration with numerous microRNAs, regulate brain cholesterol levels as well as glutamatergic and inflammatory signaling, all of which contribute to general brain homeostasis. Neural electrical activity, synaptic plasticity processes, learning, and memory are dependent on the astrocyte–neuron crosstalk. Here, we review the involvement of astrocytic microRNAs that potentially regulate cholesterol metabolism, glutamate uptake, and inflammation in Alzheimer’s disease (AD). The interaction between astrocytic microRNAs and long non-coding RNA and transcription factors specific to astrocytes also contributes to the pathogenesis of AD. Thus, astrocytic microRNAs arise as a promising target, as AD conditions are a worldwide public health problem. This review examines novel therapeutic strategies to target astrocyte dysfunction in AD, such as lipid nanodiscs, engineered G protein-coupled receptors, extracellular vesicles, and nanoparticles.
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Koyama, Yutaka. "Endothelin ETB Receptor-Mediated Astrocytic Activation: Pathological Roles in Brain Disorders." International Journal of Molecular Sciences 22, no. 9 (April 21, 2021): 4333. http://dx.doi.org/10.3390/ijms22094333.

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In brain disorders, reactive astrocytes, which are characterized by hypertrophy of the cell body and proliferative properties, are commonly observed. As reactive astrocytes are involved in the pathogenesis of several brain disorders, the control of astrocytic function has been proposed as a therapeutic strategy, and target molecules to effectively control astrocytic functions have been investigated. The production of brain endothelin-1 (ET-1), which increases in brain disorders, is involved in the pathophysiological response of the nervous system. Endothelin B (ETB) receptors are highly expressed in reactive astrocytes and are upregulated by brain injury. Activation of astrocyte ETB receptors promotes the induction of reactive astrocytes. In addition, the production of various astrocyte-derived factors, including neurotrophic factors and vascular permeability regulators, is regulated by ETB receptors. In animal models of Alzheimer’s disease, brain ischemia, neuropathic pain, and traumatic brain injury, ETB-receptor-mediated regulation of astrocytic activation has been reported to improve brain disorders. Therefore, the astrocytic ETB receptor is expected to be a promising drug target to improve several brain disorders. This article reviews the roles of ETB receptors in astrocytic activation and discusses its possible applications in the treatment of brain disorders.
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Emerson, Jacen, Thomas Delgado, Peter Girardi, and Gail V. W. Johnson. "Deletion of Transglutaminase 2 from Mouse Astrocytes Significantly Improves Their Ability to Promote Neurite Outgrowth on an Inhibitory Matrix." International Journal of Molecular Sciences 24, no. 7 (March 23, 2023): 6058. http://dx.doi.org/10.3390/ijms24076058.

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Astrocytes are the primary support cells of the central nervous system (CNS) that help maintain the energetic requirements and homeostatic environment of neurons. CNS injury causes astrocytes to take on reactive phenotypes with an altered overall function that can range from supportive to harmful for recovering neurons. The characterization of reactive astrocyte populations is a rapidly developing field, and the underlying factors and signaling pathways governing which type of reactive phenotype that astrocytes take on are poorly understood. Our previous studies suggest that transglutaminase 2 (TG2) has an important role in determining the astrocytic response to injury. Selectively deleting TG2 from astrocytes improves functional outcomes after CNS injury and causes widespread changes in gene regulation, which is associated with its nuclear localization. To begin to understand how TG2 impacts astrocytic function, we used a neuron-astrocyte co-culture paradigm to compare the effects of TG2−/− and wild-type (WT) mouse astrocytes on neurite outgrowth and synapse formation. Neurons were grown on a control substrate or an injury-simulating matrix comprised of inhibitory chondroitin sulfate proteoglycans (CSPGs). Compared to WT astrocytes, TG2−/− astrocytes supported neurite outgrowth to a significantly greater extent only on the CSPG matrix, while synapse formation assays showed mixed results depending on the pre- and post-synaptic markers analyzed. We hypothesize that TG2 regulates the supportive functions of astrocytes in injury conditions by modulating gene expression through interactions with transcription factors and transcription complexes. Based on the results of a previous yeast two-hybrid screen for TG2 interactors, we further investigated the interaction of TG2 with Zbtb7a, a ubiquitously expressed transcription factor. Co-immunoprecipitation and colocalization analyses confirmed the interaction of TG2 and Zbtb7a in the nucleus of astrocytes. Overexpression or knockdown of Zbtb7a levels in WT and TG2−/− astrocytes revealed that Zbtb7a robustly influenced astrocytic morphology and the ability of astrocytes to support neuronal outgrowth, which was significantly modulated by the presence of TG2. These findings support our hypothesis that astrocytic TG2 acts as a transcriptional regulator to influence astrocytic function, with greater influence under injury conditions that increase its expression, and Zbtb7a likely contributes to the overall effects observed with astrocytic TG2 deletion.
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Inyushin, M. Y., A. Huertas, Y. V. Kucheryavykh, L. Y. Kucheryavykh, V. Tsydzik, P. Sanabria, M. J. Eaton, S. N. Skatchkov, L. V. Rojas, and W. D. Wessinger. "L-DOPA Uptake in Astrocytic Endfeet Enwrapping Blood Vessels in Rat Brain." Parkinson's Disease 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/321406.

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Astrocyte endfeet surround brain blood vessels and can play a role in the delivery of therapeutic drugs for Parkinson’s disease. However, there is no previous evidence of the presence of LAT transporter forL-DOPA in brain astrocytes except in culture. Using systemicL-DOPA administration and a combination of patch clamp, histochemistry and confocal microscopy we found thatL-DOPA is accumulated mainly in astrocyte cell bodies, astrocytic endfeet surrounding blood vessels, and pericytes. In brain slices: (1) astrocytes were exposed to ASP+, a fluorescent monoamine analog of MPP+; (2) ASP+taken up by astrocytes was colocalized withL-DOPA fluorescence in (3) glial somata and in the endfeet attached to blood vessels; (4) these astrocytes have an electrogenic transporter current elicited by ASP+, but intriguingly not byL-DOPA, suggesting a different pathway for monoamines andL-DOPA via astrocytic membrane. (5) The pattern of monoamine oxidase (MAO type B) allocation in pericytes and astrocytic endfeet was similar to that ofL-DOPA accumulation. We conclude that astrocytes controlL-DOPA uptake and metabolism and, therefore, may play a key role in regulating brain dopamine level during dopamine-associated diseases. These data also suggest that different transporter mechanisms may exist for monoamines andL-DOPA.
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Dissertations / Theses on the topic "Astrocytes"

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Contreras-Sesvold, Carmen Sesvold Carmen Contreras. "Reactive astrocytes : phenotypic and functional characteristics and astrocytes as neural stem cells /." Download the thesis in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/ContrerasSesvold2006.pdf.

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Feresten, Abigail Helms. "Astrocytes in psychotic disorder." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45435.

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Astrocyte dysregulation has been implicated in the pathophysiology of schizophrenia (SCZ) and bipolar disorder (BPD), however the exact nature of astrocytic alterations remains to be identified. I investigated whether levels of four astrocyte-specific proteins; glial fibrillary acidic protein (GFAP), aldehyde dehydrogenase type 1L1 (ALDH1L1), vimentin, and excitatory amino acid transporter type 1 (EAAT1) are altered in SCZ and BPD. Immunohistochemical staining of ALDH1L1 and GFAP in human grey and white matter was also performed, and staining patterns compared qualitatively. Relative concentrations of GFAP, ALDH1L1, vimentin, and EAAT1 were assessed post-mortem in the dorsolateral prefrontal cortex in SCZ (n=35), BPD (n=34) and non-psychiatric control (n=35) groups by western blotting. The same proteins were also quantified in the cingulate cortex of rats administered the antipsychotics haloperidol and clozapine. Elevated levels of GFAP were observed in SCZ and BPD, when compared to controls. GFAP was also significantly increased in individuals with psychotic symptoms, when compared to those without. Vimentin, ALDH1L1 and EAAT1 levels did not differ between groups. Rats exposed to antipsychotics did not exhibit significant overall differences in any astrocytic protein, suggesting that increased GFAP in SCZ is not attributable to antipsychotic treatment. Our findings indicate that astrocyte pathology may be associated with psychotic symptoms. Lack of ALDH1L1 and vimentin variability, paired with increased GFAP levels, may imply that astrocyte numbers are unchanged but astrocytes are partially activated, or may indicate a specific dysregulation of GFAP. Immunohistochemical results suggest that ALDH1L1 may be a more reliable marker of astrocytes than GFAP in human grey matter.
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Jai-Yoon, Sul. "Calcium signalling in astrocytes." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391921.

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Škovierova, H., S. Mahmood, E. Blahovcova, J. Strnadel, J. Sopkova, and E. Halašova. "Homocystene and human astrocytes." Thesis, Сумський державний університет, 2016. http://essuir.sumdu.edu.ua/handle/123456789/44950.

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Astrocytes are multipotent and serve surprisingly large and diverse variety of functions, providing for the overall brain homeostasis, assisting in neurogenesis, determining the microarchitecture of the grey matter, and defending the brain through evolutionary conserved astrogliosis programs. Astrocytes are specifically involved in various neurodegenerative diseases, including Alzheimer’s and Parkinson’s diseases, and various forms of dementia. Homocysteine is a nonessential sulphur-containing amino acid that had been linked with neurodegenerative diseases and aging.
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James, L. R. "Calcium signal transduction in astrocytes." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.605022.

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Ca2+ signals can exhibit great spatiotemporal complexity, leading to the hypothesis that the dynamics of Ca2+ signals may allow astrocytes to discriminate between stimuli. An in vitro model system of primary cerebellar and cortical astrocytes was tailored to test this hypothesis, by comparing the kinetics of the Ca2+ signal evoked by different receptor agonists. It was found that known physiological agonists triggered highly heterogeneous responses, but there were no systematic trends in the specific kinetic parameters of Ca2+ signals that depended on the agonists which triggered them. These results suggest that the encoding of information as to agonist identity in the timing of the Ca2+ signal is unlikely to be feasible. However, different agonists vary in the efficacy with which they trigger cell-wide Ca2+ signals suggesting that there is a discrete probability that cultured astrocytes will respond to a given agonist with an all-or-none Ca2+ signal. The probability of triggering a response can be enhanced by the neuromodulator nitric oxide (NO), acting through its receptor, soluble guanylyl cyclase (sGC). The mechanism of this “gain modulation” involves activation of PKG and PKC modulating an aspect of the Gq signalling pathway in a manner that increases Ca2+ excitability. Further investigations revealed complex crosstalk between the NO and Ca2+ signalling pathways at multiple levels. In summary, the kinetics of Ca2+ signalling in cultured astrocytes while heterogeneous, do not appear to vary predictably between physiological stimuli. Instead, the probability of response does vary according to receptor agonist, and can be enhanced by co-stimulation with NO. Given the close proximity between the astrocytic endfeed and CNS capillary and neuronal networks, but of which generate NO, there is potential for this crosstalk to modulate the activity of astrocytes in vivo.
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Cambray-Deakin, M. "Astrocytes : targets for neuroactive substances." Thesis, Open University, 1985. http://oro.open.ac.uk/56910/.

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Cahoy, John David. "Genomic analysis of highly purified astrocytes reveals in vivo astrocyte gene expression : a new resource for understanding astrocyte development and function /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Mhyre, Andrew James. "Mechanisms of estrogen signaling in astrocytes /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/6266.

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Siushansian, Ramin. "Vitamin C transport by cerebral astrocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21315.pdf.

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Blaszczyk, Lucie. "Etude des cellules astrocytaires et microgliales thalamiques dans un modèle de douleur neuropathique chez le rat." Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0081/document.

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La douleur chronique est une pathologie invalidante de longue durée notamment caractériséepar trois symptômes : l’allodynie (un stimulus non douloureux est perçu comme douloureux),l’hyperalgésie (un stimulus douloureux est perçu comme encore plus douloureux) et desdouleurs ambulatoires. Quand cette douleur est due à une lésion ou une dysfonction du systèmenerveux on parle de douleur neuropathique. Chez les patients et les modèles animaux dedouleurs neuropathiques, les études ont montré que les neurones thalamiques étaienthyperexcitables. Les cellules gliales, astrocytes et microglies, sont des partenaires synaptiquesimpliqués dans la transmission et la plasticité synaptique et pourraient être impliqués dans cephénomène. En effet, ces cellules peuvent modifier leur phénotype lorsque le système nerveuxest affecté, elles sont réactives : leur morphologie est hypertrophiée, l’expression d’ARNm et deprotéines comme iba-1 (ionized binding-adaptor molecule 1) et CD11b/c (cluster ofdifferentiation 11b/c) pour les cellules microgliales et GFAP (glial fibrillary acidic protein) etS100β (S100 calcium binding protein β) pour les cellules astrocytaires est augmentée. Ellespeuvent également libérer des molécules pro-inflammatoires. Tout ceci pourrait générer ouamplifier l’hyperexcitabilité des neurones présents dans le thalamus.Mon travail de thèse a consisté en l’étude des astrocytes et de la microglie thalamique dans lemodèle de douleurs neuropathiques de ligature des nerfs spinaux L5-L6 du nerf sciatique (spinalnerve ligation, SNL). Les symptômes d’allodynie et d’hyperalgésie mécaniques ont étécaractérisés par le test des filaments de von Frey et les douleurs ambulatoires par le test dedistribution pondéral dynamique. L’expression des ARNm de marqueurs gliaux a été étudiée parune approche de qRT-PCR sur des prélèvements thalamiques et sur des noyaux thalamiquesobtenus par microdissection au laser. L’expression neurochimique des marqueurs iba-1,CD11b/c, Cathepsine S, GFAP et S100β a été étudié par immunohistofluorescence en quantifiantle nombre de cellules immunopositives et la surface occupée par les marqueurs. Toutes cesexpériences ont été réalisées à J14 et J28 après la chirurgie.A J14, les animaux SNL développent des symptômes d’allodynie et d’hyperalgésie mécaniqueainsi que des douleurs ambulatoires. Chez ces animaux, les cellules microgliales thalamiquesprésentent des signes de réactivité avec l’augmentation de l’expression des ARNm desmarqueurs CTSS et CX3CR1, le récepteur de la fractalkine, marqueurs connus pour leursimplications dans l’hyperexcitabilité neuronale spinale en conditions de douleursneuropathiques. De plus, l’expression neurochimique des marqueurs gliaux étudiés est diminuéece qui se traduit notamment par une diminution du nombre de cellules immunopositives pources marqueurs chez les animaux SNL. A J28, les symptômes douloureux sont maintenus. De plus,la réactivité microgliale décelée à J14 par qRT-PCR est toujours présente avec l’augmentation del’expression de l’ARNm codant pour la fractalkine (CX3CL1), partenaire de la voieCTSS/CX3CR1/CX3CL1. La diminution de l’expression neurochimique thalamique desmarqueurs gliaux chez les animaux SNL était transitoire et n’est plus présente à J28. Enrevanche, des signes de réactivité astrocytaire thalamique ont été mis en évidence chez lesanimaux SNL.Ainsi, ce travail dévoile une ambivalence au niveau des altérations de la glie thalamique dans cemodèle SNL: une diminution précoce de l’expression des marqueurs gliaux thalamiques suivied’une réactivité astrocytaire plus tardive concomitante à des signes de réactivité microgliale. Denombreuses expériences sont encore nécessaires pour appréhender l’impact de cetteambivalence gliale thalamique inédite dans un contexte de douleur neuropathique
Chronic pain is an incapacitating and long lasting pathology mainly characterized by threesymptoms: allodynia (a non painful stimulus is perceived as painful), hyperalgesia (a painfulstimulus is perceived as more painful) and ambulatory pains. When chronic pain is due to alesion or dysfunction of nervous system it is called neuropathic pain. In both patients and animalmodels of neuropathic pain, researchers found that thalamic neurons are hyperexcitable. Glialcells, astrocytes and microglia, are strong synaptic partners involved in synaptic transmissionand plasticity and therefore could be involved in this phenomenon. Indeed, these cells canmodify their phenotype when nervous system is damaged. They become reactive: theirmorphology is hypertrophied, mRNA and protein expression of iba-1 (ionized binding-adaptormolecule 1) and CD11b/c (cluster of differentiation 11b/c) for microglia and GFAP (glialfibrillary acidic protein) and S100β (S100 calcium binding protein β) for astrocytes is increased.They could also release pro-inflammatory molecules. All of these could contribute to generate oramplify the thalamic neuronal hyperexcitability.In my PhD work I studied thalamic astrocytes and microglia in a rat neuropathic pain model ofL5-L6 spinal nerves ligation (SNL). Mechanical allodynia and hyperalgesia were characterizedwith von Frey filament test and ambulatory pain with dynamic weight bearing apparatus. mRNAexpression of glial markers were studied with qRT-PCR technique on thalamic punches andlaser-microdissected nuclei. Neurochemical expressions of iba-1, CD11b/c, cathepsin S, GFAPand S100β markers were quantified using an immunohistofluorescence approach to count thenumber of immunopositive cells and surface stained by these markers. All these experimentswere done at D14 and D28 after surgery.At D14, SNL animals develop mechanical allodynia and hyperalgesia as well as ambulatory pain..For these animals, thalamic microglial cells showed signs of reactivity with the increase mRNAexpression of CTSS and CX3CR1, fractalkine receptor, well known markers involved in spinalneuronal hyperexcitability under neuropathic pain conditions. In addition, the number ofimmunopositive cells for the glial markers is decreased in SNL animals. At D28, the neuropathicpain symptoms are still present. Furthermore, thalamic microglial reactivity found at D14 withqRT-PCRm method is still present with the increased mRNA expression of fractalkine (CX3CL1),partner of CTSS/CX3CR1/CX3CL1 pathway. The decreased neurochemical expression of glialmarkers found at D14 was transient as I didn’t find this result at D28. However, thalamicastrocytic reactivity was found at D28 in SNL animals.So, this work reveal a new glial process at thalamic level in this SNL model of neuropathic pain :an early decreased expression of glial markers and then a later thalamic astrocytic reactivityconcomitant with signs of thalamic microglial reactivity. Numerous studies are required toexplore the role of such novel ambivalent glial alterations in the context of neuropathic pain
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Books on the topic "Astrocytes"

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Di Benedetto, Barbara, ed. Astrocytes. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9068-9.

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Milner, Richard, ed. Astrocytes. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-452-0.

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Sergey, Fedoroff, and Vernadakis Antonia 1930-, eds. Astrocytes. Orlando: Academic Press, 1986.

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1950-, Murphy Seán, ed. Astrocytes: Pharmacology and function. San Diego: Academic Press, 1993.

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Li, Baoman, Vladimir Parpura, Alexei Verkhratsky, and Caterina Scuderi, eds. Astrocytes in Psychiatric Disorders. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-77375-5.

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Astrocytes: Methods and protocols. New York: Humana Press, 2012.

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Astrocytes: Wiring the brain. Boca Raton: CRC Press, 2012.

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1954-, Schipper Hyman M., ed. Astrocytes in brain aging and neurodegeneration. Austin: R.G. Landes, 1998.

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Pérez, Oscar González. Astrocytes: Structure, functions and role in disease. New York: Nova Science Publishers, Inc., 2012.

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Gates, Jay Alan. Characterization of calmodulin from C astrocytoma cells in rat cerebrum. [New Haven: s.n.], 1986.

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Book chapters on the topic "Astrocytes"

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Rojas-Rodríguez, Felipe, Andrés Pinzón, Daniel Fuenmayor, Tábata Barbosa, Diego Vesga Jimenez, Cynthia Martin, George E. Barreto, Andrés Aristizabal-Pachón, and Janneth Gonzalez. "Multi-Omic Epigenetic-Based Model Reveals Key Molecular Mechanisms Associated with Palmitic Acid Lipotoxicity in Human Astrocyte." In Neurotoxicity - New Advances. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.100133.

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Astrocytes are critical for the metabolic, structural and functional modulatory support of the brain. Lipotoxicity or high levels of saturated fatty acid as Palmitate (PA) has been associated with neurotoxicity, the loss or change of astrocytic functionality, and the etiology and progression of neurodegenerative diseases such as Parkinson or Alzheimer. Several molecular mechanisms of PA’s effect in astrocytes have been described, yet the role of epigenetic regulation and chromatin architecture have not been fully explored. In this study, we developed a multi-omic epigenetic-based model to identify the molecular mechanisms of lipotoxic PA activity in astrocytes. We used data from nine histone modifications, location of Topological Associated Domains (TADs) and transcriptional CTCF regions, where we identified the basal astrocyte epigenetic landscape. Moreover, we integrated transcriptomic data of astrocytic cellular response to PA with the epigenetic multi-omic model to identify lipotoxic-induced molecular mechanisms. The multi-omic model showed that chromatin conformation in astrocytes treated with PA have response genes located within shared topological domains, in which most of them also showed either repressive or enhancing marks in the Chip-Seq enrichment, reinforcing the idea that epigenetic regulation has a huge impact on the lipotoxic mechanisms of PA in the brain.
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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, 32–59. 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 contribute to Alzheimer's progression, they are involved in neuroinflammation, Aβ metabolism, and calcium regulation. Conversely, in Parkinson's, astrocytes contribute to mitochondrial dysfunction, impacting dopaminergic neurons. This comprehensive exploration sheds light on the intricate and multifaceted roles of astrocytes in cognition and their potential implications for therapeutic interventions in neurological and psychiatric conditions.
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Brustle, O., and M. Dubois-Dalcq. "Stem Cells and their Gliogenic Potential." In Glial Cell Development basic principles and clinical relevance second edition, 415–36. Oxford University PressOxford, 2001. http://dx.doi.org/10.1093/oso/9780198524786.003.0020.

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Abstract A detailed understanding of the lineage relationships between the three principal cell types of the central nervous system (CNS)—neurons, astrocytes and oligodendrocytes-is a central issue in the study of CNS development and repair. The discovery that in vitro type 2 astrocytes and oligodendrocytes can develop from a common, self-renewing progenitor established the existence of a bipotential precursor for CNS glia (Raff et al., 1983; Bögler et al., 1990). These experiments also showed that the decision of a progenitor cell to differentiate into an oligodendrocyte or a type 2 astrocyte is influenced by the culture medium, indicating that the fate of neural precursor cells can be modulated by extrinsic factors. While type 2 astrocytes are rarely encountered in vivo, subsequent in vivo lineage analyses with retroviral vectors established the presence of a common progenitor for type-I astrocytes and oligodendrocytes (Levison and Goldman, 1993). These studies also provided evidence for the existence of neuron-astrocyte and neuron-oligodendrocyte precursors (Galileo et al., 1990; Williams et al., 1991). However, it was the discovery of a multipotential neural precursor cell for neurons, astrocytes and oligodendrocytes which established the neural stem cell (NSC) concept (for reviews, see Weiss et al., 1996b; McKay, 1997).
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"Front Matter." In Astrocytes, iii. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-511370-0.50001-1.

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"Copyright." In Astrocytes, iv. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-511370-0.50002-3.

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"Contributors." In Astrocytes, xv—xvii. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-511370-0.50003-5.

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Murphy, Sean. "Preface." In Astrocytes, xix—xx. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-511370-0.50004-7.

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LEVISON, STEVEN W., and JAMES E. GOLDMAN. "Astrocyte Origins." In Astrocytes, 1–22. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-511370-0.50005-9.

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SHAO, YANPING, KRISTIAN ENKVIST, and KEN McCARTHY. "Astroglial Adrenergic Receptors." In Astrocytes, 25–45. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-511370-0.50006-0.

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PEARCE, BRIAN. "Amino Acid Receptors." In Astrocytes, 47–66. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-511370-0.50007-2.

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Conference papers on the topic "Astrocytes"

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Dias, Thales Augusto Oliveira, and Silvia Graciela Ruginsk Leitão. "Participation of calcium channels in the action of angiotensin II in astrocytes." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.299.

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Background: The renin-angiotensin-aldosterone system is the main regulator of blood pressure and blood volume, with most effects being mediated by angiotensin II (Ang-II) - responsible, in the central nervous system, for actions such as thirst and sodium appetite. Astrocytes are believed to mediate such a response, as they express receptors for Ang-II and respond directly to dehydration with impacting morphological changes in the synaptic microenvironment. Many of its functions involve L-type calcium channels (LTCCs). Objectives: Evaluate the participation of LTCCs in the effects induced by AngII in cultured hypothalamic astrocytes. Methods: The effect of incubation with verapamil on the morphological responses induced by Ang-II was evaluated in hypothalamic astrocyte culture, by analyzing the expression of the cytoskeletal protein GFAP and the cell viability by the MTT assay, by immunofluorescence. Results: Incubation with Ang-II reduced the cell area considerably due to GFAP expression in relation to the control group (DMEM p<0.001), indicating that the results observed on GFAP expression did not result from cell death. Conclusion: Incubation with Ang-II alters the astrocyte morphology, reducing its area, effect at least in part, blocked by the action of Verapamil, indicating the participation of LTCCs in the mediation of this process.
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Rocha, Andreia, Bruna Bellaver, Luiza Machado, Carolina Soares, Pâmela C. L. Ferreira, Samuel Greggio Gianina T. Venturin, Jaderson C. da Costa, Diogo O. Souza, and Eduardo R. Zimmer. "TEMPORAL CHANGES IN ASTROCYTES ON A TRANSGENIC RAT MODEL OF AD." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda023.

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Background: Recent evidences have pointed to astrocytes as important players in the Alzheimer’s Disease (AD) pathogenesis. Objective: With this in mind, we aim to longitudinally investigate astrocyte changes in a new important AD transgenic model, the TgF344-AD rat, the first animal model harboring human APP/PS1 mutations which presents age-dependent amyloid and tau pathology. Methods: TgF344-AD rats and wild type littermates were evaluated in three time points: 3, 6 and 9 months of age. Rats underwent a [18F]FDG-microPET, a spatial-memory, an astrocytes CSF biomarkers (ELISA multiplex) and a glutamate uptake (ex-vivo slices) analysis. Examination of further time-points are being conducted at the moment. Results: At 9 months of age, TgF344-AD animals presented an increase in the cortical [18F]FDG uptake and a decline in their alternance performance in the Y-maze task. In the CSF analysis, GFAP was elevated at both 6 months and 9 months, while S100B presented a decrease at 6mo. Additionally, the cortical glutamate uptake was increased at 9 months. Conclusion: This study is the first to longitudinally investigate the in vivo brain glucose metabolism in the TgF344-AD rat model. Our results suggest that this model presents an early increase on glucose metabolism which may be related to astrocytes activation and the increase of glutamate uptake by these cells. Furthermore, we also identified a spatial memory impairment at the same age.
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Bernick, Kristin B., and Simona Socrate. "Substrate Dependence of Mechanical Response of Neurons and Astrocytes." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53538.

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The response of neural cells to mechanical cues is a critical component of the innate neuroprotective cascade aimed at minimizing the consequences of traumatic brain injury (TBI). Reactive gliosis and the formation of glial scars around the lesion site are among the processes triggered by TBI where mechanical stimuli play a central role. It is well established that the mechanical properties of the microenvironment influence phenotype and morphology in most cell types. It has been shown that astrocytes change morphology [1] and cytoskeletal content [2] when grown on substrates of varying stiffness, and that mechanically injured astrocyte cultures show alterations in cell stiffness [3]. Accurate estimates of the mechanical properties of central nervous system (CNS) cells in their in-vivo conditions are needed to develop multiscale models of TBI. Lu et al found astrocytes to be softer than neurons under small deformations [4]. In recent studies, we investigated the response of neurons to large strains and at different loading rates in order to develop single cell models capable of simulating cell deformations in regimes relevant for TBI conditions [5]. However, these studies have been conducted on cells cultured on hard substrates, and the measured cell properties might differ from their in-vivo counterparts due to the aforementioned effects. Here, in order to investigate the effects of substrate stiffness on the cell mechanical properties, we used atomic force microscopy (AFM) and confocal imaging techniques to characterize the response of primary neurons and astrocytes cultured on polyacrylamide (PAA) gels of varying composition. The use of artificial gels minimizes confounding effects associated with biopolymer gels (both protein-based and polysaccharide-based) where specific receptor bindings may trigger additional biochemical responses [1].
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Ravagnani, Felipe, Hellen Valerio, Jersey Maués, Arthur de Oliveira, Renato Puga, Karina Oliveira, Fabíola Picosse, et al. "Omics profile of iPSC-derived astrocytes from Progressive Supranuclear Palsy (PSP) patients." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.414.

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Progressive Supranuclear Palsy (PSP) is a neurodegenerative tauopathy and, to date, the pathophysiological mechanisms in PSP that lead to Tau hyperphosphorylation and neurodegeneration are not clear. The development of a model using neural cell lines derived from patients has the potential to identify molecules and possible biomarkers. We developed a model of induced pluripotent stem cells iPSC-derived astrocytes to investigate the pathophysiology of PSP, particularly early events that might contribute to Tau hyperphosphorylation, applying an omics approach to detect differentially expressed genes, metabolites, and proteins, including those from the secretome. Skin fibroblasts from PSP patients and controls were reprogrammed to iPSCs, which were further differentiated into neuroprogenitor cells and astrocytes. In the 5th passage, astrocytes were harvested for total ribonucleic acid sequencing. Intracellular and secreted proteins were processed for proteomics experiments. Metabolomics profiling was obtained from supernatants only. We identified hundreds of differentially expressed genes in PSP. The main networks were related to cell cycle activation. Several proteins were found exclusively secreted by the PSP group. The cellular processes related to the cell cycle and mitotic proteins, chaperonins of the TriC/CCT pathway, and redox signaling are enriched in the secretome of the PSP group. Moreover, we found spatial segregation by PCA in the metabolomics data, indicating distinct sets of metabolites between PSP and control groups. Our iPSC-derived astrocyte model can provide distinct molecular signatures for PSP patients and it is useful to elucidate the initial stages of PSP pathogenesis.
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Pletnikov, Mikhail V. "ASTROCYTES IN COGNITIVE DYSFUNCTION." In MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-7.

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Leung, Lai Yee, Pamela J. VandeVord, Warren Hardy, Roche De Guzman, King H. Yang, and Albert I. King. "Effects of Short Duration Overpressure on Astrocytes: An In Vitro Study." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176202.

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Blast wave overpressure from detonations can injure physiological systems ‘silently.’ Experimental and clinical studies have revealed the damaging effects of shock waves on different physiological systems, such as ears, lungs and gastrointestinal tracts [1, 2]. Despite the improved helmet and body armor, many veterans returning from wars suffered from neurological disorders that are being diagnosed as mild traumatic brain injury. Warden (2006) reported that most of these veterans were exposed to blast [3]. In vivo study illustrated neuronal degeneration in the brain after exposure to blast waves [4]. As with many neuronal diseases, blast-induced neuronal injury may be related to microglia and astrocyte activation. However, the underlying mechanism is not clearly understood. This study was aimed at investigating the effects of short duration overpressure on astrocytes, in terms of cell proliferation and mRNA expression of several apoptotic genes and glial fibrillary acidic protein (GFAP).
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Tang, Guangzhi, Ioannis E. Polykretis, Vladimir A. Ivanov, Arpit Shah, and Konstantinos P. Michmizos. "Introducing Astrocytes on a Neuromorphic Processor." In the 7th Annual Neuro-inspired Computational Elements Workshop. New York, New York, USA: ACM Press, 2019. http://dx.doi.org/10.1145/3320288.3320302.

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Erkan, Yasemin, Mahmut Ozer, and Ergin Yilmaz. "Effects of astrocytes on neuronal dynamics." In 2017 Medical Technologies National Congress (TIPTEKNO). IEEE, 2017. http://dx.doi.org/10.1109/tiptekno.2017.8238069.

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Liu, Xin. "Research on astrocytes regulate sleep mechanisms." In Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), edited by Alan Wang. SPIE, 2024. http://dx.doi.org/10.1117/12.3013058.

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Makovkin, Sergey, Mikhail Ivanchenko, and Susanna Gordleeva. "Neuronal intermittent synchronization enhanced by astrocytes." In 2022 6th Scientific School Dynamics of Complex Networks and their Applications (DCNA). IEEE, 2022. http://dx.doi.org/10.1109/dcna56428.2022.9923142.

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Reports on the topic "Astrocytes"

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Yang, Lin, Yanzhu Liu, Trudy M. Forte, Jeffrey W. Chisholm, John S. Parks, and Neil S. Shachter. Cultured human astrocytes secrete large cholesteryl ester- andtriglyceride-rich lipoproteins along with endothelial lipase. Office of Scientific and Technical Information (OSTI), December 2003. http://dx.doi.org/10.2172/886608.

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Elmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.
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Li, Nianzhen. Nitric Oxide in Astrocyte-Neuron Signaling. Office of Scientific and Technical Information (OSTI), January 2002. http://dx.doi.org/10.2172/803739.

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Sulzer, David. Altered Astrocyte-Neuron Interactions and Epileptogenesis in Tuberous Sclerosis Complex Disorder. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada610226.

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Maragakis, Nicholas J., and Hongjun Song. Preclinical Studies of Induced Pluripotent Stem Cell-Derived Astrocyte Transplantation in ALS. Fort Belvoir, VA: Defense Technical Information Center, December 2014. http://dx.doi.org/10.21236/ada613757.

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Maragakis, Nicholas J., and Hongjun Song. Preclinical Studies of Induced Pluripotent Stem Cell-Derived Astrocyte Transplantation in ALS. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada568166.

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Maragakis, Nicholas J., and Hongjun Song. Preclinical Studies of Induced Pluripotent Stem Cell-Derived Astrocyte Transplantation in ALS. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada555307.

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Kahler, David W., and Carmen M. Arroyo. Normal Human Astrocyte Instructions for Initiation of Cultures from Cryopreserved Cells and Subculture. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada442897.

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Mahmoudi, Farhad, Mahtab Mokarram, Sadegh Sabouhi, Sara Hashemi, Parastoo Saberi, and Hadi Zamanian. Application of digital health for improving medication adherence in MS patients. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0058.

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Review question / Objective: The aim of this study is to evaluate the efficacy of digital health interventions in monitoring and improving medication adherence in Multiple Sclerosis patients. Condition being studied: Multiple sclerosis (MS) is the most prevalent chronic inflammatory disease of the central nervous system (CNS), which leads to focal lesions in the white matter, characterized by selective primary demyelination with partial preservation of axons and reactive astrocytic gliosis. The disease is thought to be due to a complex interaction between different genetic and environmental factors. The prevalence of MS is rising all over the world, due on one hand to earlier diagnosis and prolonged survival, and on the other to a true increase in incidence of the disease. The diagnosis of MS remains clinical despite recent advances in diagnostics and relies on demonstrating dissemination in space and time while excluding alternative diagnoses.
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Huang, Yujie. Characterizing and Targeting Bone Marrow-Derived Inflammatory Cells in Driving the Malignancy and Progression of Childhood Astrocytic Brain Tumors. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada614183.

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