Relevant bibliographies by topics / Astrocyte

Academic literature on the topic 'Astrocyte'

Author: Grafiati
Published: 4 June 2021
Last updated: 14 March 2023

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Journal articles on the topic "Astrocyte"

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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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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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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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Rosa, Juao-Guilherme, Katherine Hamel, Carrie Sheeler, Ella Borgenheimer, Stephen Gilliat, Alyssa Soles, Ferris J. Ghannoum, et al. "Spatial and Temporal Diversity of Astrocyte Phenotypes in Spinocerebellar Ataxia Type 1 Mice." Cells 11, no. 20 (October 21, 2022): 3323. http://dx.doi.org/10.3390/cells11203323.

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While astrocyte heterogeneity is an important feature of the healthy brain, less is understood about spatiotemporal heterogeneity of astrocytes in brain disease. Spinocerebellar ataxia type 1 (SCA1) is a progressive neurodegenerative disease caused by a CAG repeat expansion in the gene Ataxin1 (ATXN1). We characterized astrocytes across disease progression in the four clinically relevant brain regions, cerebellum, brainstem, hippocampus, and motor cortex, of Atxn1154Q/2Q mice, a knock-in mouse model of SCA1. We found brain region-specific changes in astrocyte density and GFAP expression and area, early in the disease and prior to neuronal loss. Expression of astrocytic core homeostatic genes was also altered in a brain region-specific manner and correlated with neuronal activity, indicating that astrocytes may compensate or exacerbate neuronal dysfunction. Late in disease, expression of astrocytic homeostatic genes was reduced in all four brain regions, indicating loss of astrocyte functions. We observed no obvious correlation between spatiotemporal changes in microglia and spatiotemporal astrocyte alterations, indicating a complex orchestration of glial phenotypes in disease. These results support spatiotemporal diversity of glial phenotypes as an important feature of the brain disease that may contribute to SCA1 pathogenesis in a brain region and disease stage-specific manner.
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Birck, Cindy, Aurélien Ginolhac, Maria Angeliki S. Pavlou, Alessandro Michelucci, Paul Heuschling, and Luc Grandbarbe. "NF-κB and TNF Affect the Astrocytic Differentiation from Neural Stem Cells." Cells 10, no. 4 (April 8, 2021): 840. http://dx.doi.org/10.3390/cells10040840.

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The NF-κB signaling pathway is crucial during development and inflammatory processes. We have previously shown that NF-κB activation induces dedifferentiation of astrocytes into neural progenitor cells (NPCs). Here, we provide evidence that the NF-κB pathway plays also a fundamental role during the differentiation of NPCs into astrocytes. First, we show that the NF-κB pathway is essential to initiate astrocytic differentiation as its early inhibition induces NPC apoptosis and impedes their differentiation. Second, we demonstrate that persistent NF-κB activation affects NPC-derived astrocyte differentiation. Tumor necrosis factor (TNF)-treated NPCs show NF-κB activation, maintain their multipotential and proliferation properties, display persistent expression of immature markers and inhibit astrocyte markers. Third, we analyze the effect of NF-κB activation on the main known astrocytic differentiation pathways, such as NOTCH and JAK-STAT. Our findings suggest that the NF-κB pathway plays a dual fundamental role during NPC differentiation into astrocytes: it promotes astrocyte specification, but its persistent activation impedes their differentiation.
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Peteri, Ulla-Kaisa, Juho Pitkonen, Kagistia Hana Utami, Jere Paavola, Laurent Roybon, Mahmoud A. Pouladi, and Maija L. Castrén. "Generation of the Human Pluripotent Stem-Cell-Derived Astrocyte Model with Forebrain Identity." Brain Sciences 11, no. 2 (February 9, 2021): 209. http://dx.doi.org/10.3390/brainsci11020209.

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Astrocytes form functionally and morphologically distinct populations of cells with brain-region-specific properties. Human pluripotent stem cells (hPSCs) offer possibilities to generate astroglia for studies investigating mechanisms governing the emergence of astrocytic diversity. We established a method to generate human astrocytes from hPSCs with forebrain patterning and final specification with ciliary neurotrophic factor (CNTF). Transcriptome profiling and gene enrichment analysis monitored the sequential expression of genes determining astrocyte differentiation and confirmed activation of forebrain differentiation pathways at Day 30 (D30) and D60 of differentiation in vitro. More than 90% of astrocytes aged D95 in vitro co-expressed the astrocytic markers glial fibrillary acidic protein (GFAP) and S100β. Intracellular calcium responses to ATP indicated differentiation of the functional astrocyte population with constitutive monocyte chemoattractant protein-1 (MCP-1/CCL2) and tissue inhibitor of metalloproteinases-2 (TIMP-2) expression. The method was reproducible across several hPSC lines, and the data demonstrated the usefulness of forebrain astrocyte modeling in research investigating forebrain pathology.
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Sulimai, Nurul, Jason Brown, and David Lominadze. "Fibrinogen Interaction with Astrocyte ICAM-1 and PrPC Results in the Generation of ROS and Neuronal Death." International Journal of Molecular Sciences 22, no. 5 (February 27, 2021): 2391. http://dx.doi.org/10.3390/ijms22052391.

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Many neuroinflammatory diseases, like traumatic brain injury (TBI), are associated with an elevated level of fibrinogen and short-term memory (STM) impairment. We found that during TBI, extravasated fibrinogen deposited in vasculo-astrocyte interfaces, which was associated with neurodegeneration and STM reduction. The mechanisms of this fibrinogen-astrocyte interaction and its functional role in neurodegeneration are still unclear. Cultured mouse brain astrocytes were treated with fibrinogen in the presence or absence of function-blocking antibody or peptide against its astrocyte receptors intercellular adhesion molecule-1 (ICAM-1) or cellular prion protein (PrPC), respectively. Fibrinogen interactions with astrocytic ICAM-1 and PrPC were characterized. The expression of pro-inflammatory markers, generations of reactive oxygen species (ROS) and nitric oxide (NO) in astrocytes, and neuronal death caused by astrocyte-conditioned medium were assessed. Data showed a strong association between fibrinogen and astrocytic ICAM-1 or PrPC, overexpression of pro-inflammatory cytokines and overproduction of ROS and NO, resulting in neuronal apoptosis and death. These effects were reduced by blocking the function of astrocytic ICAM-1 and PrPC, suggesting that fibrinogen association with its astrocytic receptors induce the release of pro-inflammatory cytokines, resulting in oxidative stress, and ultimately neuronal death. This can be a mechanism of neurodegeneration and the resultant STM reduction seen during TBI.
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Haydon, Philip G., and Giorgio Carmignoto. "Astrocyte Control of Synaptic Transmission and Neurovascular Coupling." Physiological Reviews 86, no. 3 (July 2006): 1009–31. http://dx.doi.org/10.1152/physrev.00049.2005.

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From a structural perspective, the predominant glial cell of the central nervous system, the astrocyte, is positioned to regulate synaptic transmission and neurovascular coupling: the processes of one astrocyte contact tens of thousands of synapses, while other processes of the same cell form endfeet on capillaries and arterioles. The application of subcellular imaging of Ca2+ signaling to astrocytes now provides functional data to support this structural notion. Astrocytes express receptors for many neurotransmitters, and their activation leads to oscillations in internal Ca2+. These oscillations induce the accumulation of arachidonic acid and the release of the chemical transmitters glutamate, d-serine, and ATP. Ca2+ oscillations in astrocytic endfeet can control cerebral microcirculation through the arachidonic acid metabolites prostaglandin E2 and epoxyeicosatrienoic acids that induce arteriole dilation, and 20-HETE that induces arteriole constriction. In addition to actions on the vasculature, the release of chemical transmitters from astrocytes regulates neuronal function. Astrocyte-derived glutamate, which preferentially acts on extrasynaptic receptors, can promote neuronal synchrony, enhance neuronal excitability, and modulate synaptic transmission. Astrocyte-derived d-serine, by acting on the glycine-binding site of the N-methyl-d-aspartate receptor, can modulate synaptic plasticity. Astrocyte-derived ATP, which is hydrolyzed to adenosine in the extracellular space, has inhibitory actions and mediates synaptic cross-talk underlying heterosynaptic depression. Now that we appreciate this range of actions of astrocytic signaling, some of the immediate challenges are to determine how the astrocyte regulates neuronal integration and how both excitatory (glutamate) and inhibitory signals (adenosine) provided by the same glial cell act in concert to regulate neuronal function.
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Tedeschi, B., J. N. Barrett, and R. W. Keane. "Astrocytes produce interferon that enhances the expression of H-2 antigens on a subpopulation of brain cells." Journal of Cell Biology 102, no. 6 (June 1, 1986): 2244–53. http://dx.doi.org/10.1083/jcb.102.6.2244.

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Using primary culture methods, we show that purified astrocytes from embryonic mouse or rat central nervous system (CNS) can be induced to produce interferon (IFN) activity when pretreated with a standard IFN-superinducing regimen of polyribonucleotide, cycloheximide, and actinomycin D, whereas IFN activity was not inducible in neuronal cultures derived from mouse CNS. Astrocyte IFN displays inductive, kinetic, physicochemical, and antigenic properties similar to those of IFN-alpha/beta, but is dissimilar to lymphocyte IFN (IFN-gamma). Treatment of pure astrocytic cultures or astrocytes cultured with neurons with astrocyte IFN or IFN-alpha/beta induced a dramatic increase in the expression of H-2 antigens on a subpopulation of astrocytes. Neither neurons nor oligodendroglia expressed detectable levels of H-2 antigens when exposed to astrocyte IFN, IFN-alpha/beta, or to IFN-beta. Injection of astrocyte IFN or IFN-alpha/beta directly into brains of newborn mice indicated that H-2 antigens were also induced in vivo. None of the IFNs (astrocyte, alpha/beta, or beta) tested induced Ia antigens on CNS cells in vitro or in vivo. Since H-2 antigens have a critical role in immune responses, astrocyte IFN may initiate and participate in immune reactions that contribute to immunoprotective and immunopathological responses in the CNS.
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Dissertations / Theses on the topic "Astrocyte"

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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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Adcock, K. H. "Astrocytic inhibition of neurite outgrowth at the Schwann cell/astrocyte interface." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.595362.

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The objectives of this thesis are to create a simplified in vitro model that mimics the neurite behaviour at the interface between the CNS and PNS and to overcome the repulsion by astrocytes. This has been achieved by co-culturing astrocytes and Schwann cells and monitoring neurite behaviour on them. In such a model neurites extending from a dorsal root ganglion explant exhibit a preference for Schwann cells and rarely cross the interface to grow onto astrocytes demonstrating that there is similarly between the model and the in vivo situation. Various molecules have been implicated in the guidance of neurite trajectories and several classes of these have been investigated in the course of this thesis. Two classes of molecules have been identified as having a role in guiding neurites at the Schwann cell/astrocyte interface: the first a cell adhesion molecule, L1, the second requires intracellular signalling events to be triggered by a neurotrophin and cyclic AMP. The production and regulation of a class of protease inhibitors, the TIMP family, by astrocytes in vivo and in vitro was also investigated. Astrocytes make at least 3 of these proteins which could also contribute to the general lack of neurite outgrowth seen on astrocytes when there is a choice between Schwann cells and astrocytes.
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Ghezali, Grégory. "Control of synaptic transmission by astroglial connexin 30 : molecular basis, activity-dependence and physiological implication." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066423/document.

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Les astrocytes périsynaptiques participent activement, au côté des neurones, dans le traitement de l’information cérébrale. Une propriété essentielle des astrocytes est d’exprimer un niveau élevé de protéines appelées connexines (Cxs), et formant les sous-unités des jonctions communicantes. Étonnamment, bien qu’il ait été suggéré très tôt que la Cx30 astrocytaire soit impliquée dans des processus cognitifs, son rôle exact dans la neurophysiologie demeure cependant encore mal connu. Nous avons récemment révélé que la Cx30, via une fonction non-canal inédite, contrôle la force et la plasticité de la transmission synaptique glutamatergique de l’hippocampe en régulant les niveaux synaptiques de glutamate par le biais du transport astrocytaire du glutamate. Cependant, les mécanismes moléculaire et cellulaire impliqués dans ce contrôle, ainsi que sa régulation dynamique par l’activité neuronale et son impact in vivo dans un contexte physiologique restaient inconnus. Dans le cadre de cette problématique, j’ai démontré durant ma thèse que: 1) La Cx30 induit la maturation morphologique des astrocytes de l’hippocampe par l’intermédiaire de la modulation d’une voie de signalisation dépendante de la laminine et régulant la polarisation cellulaire ; 2) l’expression de la Cx30, sa localisation perisynaptique, ainsi que ses fonctions sont modulées par l’activité neuronale ; 3) Le contrôle de la couverture astrocytaire des synapses du noyau supraoptique de l’hypothalamus par la Cx30 fixe les niveaux plasmatiques de base de la neurohormone ocytocine et ainsi favorise la mise en place de comportements sociaux adaptés. Dans l’ensemble, ces résultats éclairent les régulations des Cxs astrocytaires par l’activité neuronale et leur rôle dans le développement postnatal des réseaux neurogliaux, ainsi que dans le contrôle des interactions structurelles astrocytes-synapses à l’origine de processus comportementaux
Perisynaptic astrocytes are active partners of neurons in cerebral information processing. A key property of astrocytes is to express high levels of the gap junction forming proteins, the connexins (Cxs). Strikingly, astroglial Cx30 was suggested early on to be involved in cognitive processes; however, its specific role in neurophysiology has yet been unexplored. We recently reveal that Cx30, through an unconventional non-channel function, controls hippocampal glutamatergic synaptic strength and plasticity by directly setting synaptic glutamate levels through astroglial glutamate clearance. Yet the cellular and molecular mechanisms involved in such control, its dynamic regulation by activity and its impact in vivo in a physiological context were unknown. To answer these questions, I demonstrated during my PhD that: 1) Cx30 drives the morphological maturation of hippocampal astrocytes via the modulation of a laminin signaling pathway regulating cell polarization; 2) Cx30 expression, perisynaptic localization and functions are modulated by neuronal activity; 3) Cx30-mediated control of astrocyte synapse coverage in the supraoptic nucleus of the hypothalamus sets basal plasmatic level of the neurohormone oxytocin and hence promotes appropriate oxytocin-based social abilities. Taken together, these data shed new light on astroglial Cxs activity-dependent regulations and roles in the postnatal development of neuroglial networks, as well as in astrocyte-synapse structural interactions mediating behavioral processes
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Stringer, Charles Edward Alexander. "Calcium dependent astrocyte-neuron communication." Thesis, University of British Columbia, 2007. http://hdl.handle.net/2429/32690.

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The discovery of direct communication between astrocytes and neurons has changed the perception of astrocytes from passive support cells to active partners in information processing. Astrocytes express myriad neurotransmitter receptors and have been shown to release neurotransmitters, allowing these cells to respond and signal to adjacent neurons, respectively. Astrocytes can rapidly respond to neurotransmitters with a rise in [Ca²⁺]i and astrocyte neurotransmitter release has been shown to be calcium dependent. The purpose of this research was to investigate unknown aspects of astrocyteneuron communication with in situ calcium imaging to improve our understanding of how these cells interact functionally. The first objective of this research was to determine whether extracellular dopamine elicits astrocyte calcium transients in the prefrontal cortex (PFC). Astrocytes from this area express dopamine receptors and dopamine is an important neurotransmitter in the PFC. We found that astrocytes in PFC brain slices reliably respond to a high concentration of dopamine ([50μM]) with [Ca²⁺]i transients, however these responses were due to the activation of adrenoreceptors, not dopamine receptors. The inability of a lower concentration of dopamine ([10μM]) to elicit astrocyte [Ca²⁺]i transients questions the whether these cells can rapidly respond to PFC dopamine at physiological levels. The second objective of this research was to investigate the extent that calcium dependent glutamate release from astrocytes is able to influence neural activity. The best studied mechanism of astrocyte gliotransmitter release is the calcium dependent release of glutamate which has been demonstrated in single astrocytes in situ. We used the vasoactive peptide endothelin to preferentially elicit widespread astrocyte [Ca²⁺]i transients astrocytes from hippocampal brain slices to determine whether the widespread calcium rise in astrocytes was associated with a change in glutamate sensitive synaptic transmission. Despite eliciting nearly ubiquitous astrocyte calcium responses, we observed no change in glutamate sensitive synaptic transmission as measured by extracellular field recordings. These results question the ability of astrocytes to acutely influence synaptic transmission of a brain region. Our findings do not support an acute role of calcium dependent communication between astrocytes and neurons in rapid information processing in the systems we investigated.
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Smith, Maria Civita. "MAPPING ASTROCYTE DEVELOPMENT IN THE DORSAL CORTEX OF THE MOUSE BRAIN." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1373039738.

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Stewart, Courtney Elizabeth. "Astrocyte Development and Function is FGF8 Signaling Dependent." Kent State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=kent1556290142104336.

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Thorén, Anna. "Astrocyte metabolism following focal cerebral ischemia /." Göteborg : Institute of Neuroscience and Physiology, The Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/744.

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Boycott, Hannah Elizabeth. "Hypoxic modulation of astrocyte glutamate transporters." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.445941.

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Johnstone, S. R. "Rodent astrocyte sub-types in vitro." Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37737.

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PELASSA, SIMONE. "Signalling from astrocyte processes in CNS." Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1043545.

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The role of astrocytes in the Central Nervous System (CNS) has been increasingly recognized in the last decades. Astrocytes, indeed, not only support neurons but also play a key role in signal transmission in CNS releasing gliotransmitters as glutamate and participating to the tripartite synpases. Here, astrocytes function in signal transmission was modeled using ex-vivo models purified from adult rat brain, named gliosomes. Using the perfusion technique, release from gliosomes was tested in three different contexts: - glutamate release associated to receptor-receptor interactions, - exosomes release, - glutamate release evoked by photobiomodulation stimulation.
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Books on the topic "Astrocyte"

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Baorto, David M. Induction and growth of astrocyte processes. [New York]: Columbia University, 1992.

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Fedoroff, Sergey, Bernhard H. J. Juurlink, and Ronald Doucette, eds. Biology and Pathology of Astrocyte-Neuron Interactions. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4757-9486-1.

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Sergey, Fedoroff, Juurlink, B. H. J., 1947-, Doucette Ronald, and Altschul Symposium (2nd : 1992 : Saskatoon, Sask.), eds. Biology and pathology of astrocyte-neuron interactions. New York: Plenum Press, 1993.

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Ikiz, Burcin. Unraveling the molecular mechanism underlying ALS-linked astrocyte toxicity for motor neurons. [New York, N.Y.?]: [publisher not identified], 2013.

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Ju, William Young-Ho. Characterization and manipulation of the reactive astrocyte response following axotomy-induced motoneuronal injury and death. Ottawa: National Library of Canada, 1994.

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Kang, Woo Hyeun. Reducing the Societal Costs of Traumatic Brain Injury: Astrocyte-Based Therapeutics and Functional Injury Tolerance of the Living Brain. [New York, N.Y.?]: [publisher not identified], 2014.

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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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Gutowski, Nicholas Jan. Cellular and molecular studies related to a cell line of the oligodendrocyte-type-2 astrocyte lineage derived from a human glioblastoma multiforme. Birmingham: University of Birmingham, 1995.

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Book chapters on the topic "Astrocyte"

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Levison, Steven W., Jean de Vellis, and James E. Goldman. "Astrocyte Development." In Developmental Neurobiology, 197–222. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-28117-7_7.

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McIver, Sally R., Mathilde Faideau, and Philip G. Haydon. "Astrocyte–Neuron Communications." In Neural-Immune Interactions in Brain Function and Alcohol Related Disorders, 31–64. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4729-0_2.

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Gorman, Julia, Konstantin Holzhausen, Joyce Reimer, and Jørgen Riseth. "Realizing Synaptic Signal Transmission During Astrocyte-Neuron Interactions within the EMI Framework." In Computational Physiology, 65–78. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-25374-4_5.

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AbstractThe tripartite synapse or “neural threesome” refers to the interplay in the synapse between neighbouring neurons, the synaptic cleft, and the surrounding glial cells. Despite extensive research, the effects of glial cells, such as astrocytes, on signal transduction between neurons are not fully understood. The Kirchhoff-Nernst- Planck (KNP) and Extracellular-Membrane-Intracellular (EMI) models constitute a promising framework for modeling these kinds of systems. However, they lack the neurotransmitter-related mechanisms that are necessary to bridge signal transduction across the synaptic cleft. Here, we propose an extension to the KNP-EMI model by a spatio-temporal diffusion-based description of the most prominent neurotransmitter, glutamate, that allows for investigation of the contribution of astrocytes to the functionality of the synapse. We validate our model by showing that the presence of an astrocyte in the domain affects the glutamate flux across the postsynaptic terminal, as observed physiologically. The proposed extension offers a sufficiently simple way of integrating synaptic glutamate dynamics into the KNP-EMI framework. It introduces the relevant interactions between electrical activity and diffusion processes at the tripartite synapse that are necessary to assess how astrocytes might contribute to the functionality of the synapse. This work has implications for future studies involving glial mechanisms and other charged species within the KNP-EMI framework.
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Ben Chikha, Soukeina, Kirmene Marzouki, and Samir Ben Ahmed. "Modeling Astrocyte-Neuron Interactions." In Neural Information Processing, 306–14. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-26555-1_35.

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Cole, Ruth, and Jean de Vellis. "Astrocyte and Oligodendrocyte Cultures." In Protocols for Neural Cell Culture, 117–30. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-2586-5_8.

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Kimelberg, Harold K. "Astrocyte Heterogeneity or Homogeneity?" In Astrocytes in (Patho)Physiology of the Nervous System, 1–25. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-79492-1_1.

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Guizzetti, Marina, Terrance J. Kavanagh, and Lucio G. Costa. "Measurements of Astrocyte Proliferation." In Methods in Molecular Biology, 349–59. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-170-3_24.

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Nishiyama, Akiko. "Astrocyte Differentiation from Oligodendrocyte Precursors." In Emerging Concepts in Neuro-Oncology, 41–60. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-458-6_3.

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Gordon, Grant R. J., Sean J. Mulligan, and Brian A. MacVicar. "Astrocyte control of blood flow." In Astrocytes in (Patho)Physiology of the Nervous System, 461–86. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-79492-1_18.

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Afshari, Fardad T., and James W. Fawcett. "Astrocyte–Schwann-Cell Coculture Systems." In Methods in Molecular Biology, 381–91. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-452-0_25.

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Conference papers on the topic "Astrocyte"

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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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Genocchi, Barbara, Annika Ahtiainen, Michael T. Barros, Jarno M. A. Tanskanen, Jari Hyttinen, and Kerstin Lenk. "Astrocytic control in in vitro and simulated neuron-astrocyte networks." In NANOCOM '21: The Eighth Annual ACM International Conference on Nanoscale Computing and Communication. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3477206.3477458.

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Ivanchenko, Mikhail, Mikhail Krivonosov, Dmitriy Burmistrov, Elena Mitroshina, Tatiana Mishchenko, and Maria Vedunova. "Analysis of time lapse imaging of astrocyte calcium activity and reconstruction of astrocytic networks." In 2020 4th Scientific School on Dynamics of Complex Networks and their Application in Intellectual Robotics (DCNAIR). IEEE, 2020. http://dx.doi.org/10.1109/dcnair50402.2020.9216871.

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Suwannatat, P., G. Luna, B. Ruttenberg, R. Raviv, G. Lewis, S. K. Fisher, and T. Hollerer. "Interactive visualization of retinal astrocyte images." In 2011 8th IEEE International Symposium on Biomedical Imaging (ISBI 2011). IEEE, 2011. http://dx.doi.org/10.1109/isbi.2011.5872397.

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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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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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Irizarry-Valle, Yilda, and Alice C. Parker. "Astrocyte on neuronal phase synchrony in CMOS." In 2014 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2014. http://dx.doi.org/10.1109/iscas.2014.6865115.

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Tsybina, Yuliya, Mikhail Krivonosov, Susan Gordleeva, Alexey Zaikin, and Alexander Gorban. "Short-term memory in neuron-astrocyte network." In 2020 4th Scientific School on Dynamics of Complex Networks and their Application in Intellectual Robotics (DCNAIR). IEEE, 2020. http://dx.doi.org/10.1109/dcnair50402.2020.9216909.

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Tsybina, Yuliya, Susan Gordleeva, Mikhail Krivonosov, Innokentiy Kastalskiy, Alexey Zaikin, and Alexander Gorban. "Modelling working memory in neuron-astrocyte network." In 2021 International Joint Conference on Neural Networks (IJCNN). IEEE, 2021. http://dx.doi.org/10.1109/ijcnn52387.2021.9533307.

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Abed, Bassam Abdul-Rahman, Amelia Ritahani Ismail, and Normaziah Abdul Aziz. "Real time astrocyte in spiking neural network." In 2015 SAI Intelligent Systems Conference (IntelliSys). IEEE, 2015. http://dx.doi.org/10.1109/intellisys.2015.7361196.

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Reports on the topic "Astrocyte"

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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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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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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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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 2015. http://dx.doi.org/10.21236/ada622431.

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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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