57,519 results match your criteria astrocytes


Shenqi Yizhi Granule attenuates Aβ induced cognitive dysfunction via inhibiting JAK2/STAT3 activated astrocyte reactivity.

Exp Gerontol 2021 May 8:111400. Epub 2021 May 8.

Institute of Meterial Medica Integration and Transformation for Brain Disorders, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, PR China; School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, PR China. Electronic address:

Shenqi Yizhi Granule (SYG), a modern preparation herbs based on the theory of traditional Chinese medicine, has been proved to be effective against Alzheimer's disease in clinical trials, APP/PS1 mice and 5XFAD transgenic mice. But the underlying mechanism remains ambiguous. Increasing evidence supports the crucial role of astrocyte reactivity in the pathogenesis of Alzheimer's disease (AD). Read More

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SREBP2 gene therapy targeting striatal astrocytes ameliorates Huntington's disease phenotypes.

Brain 2021 May 11. Epub 2021 May 11.

Department of Biosciences, University of Milan, 20133, Milan, Italy.

Brain cholesterol is produced mainly by astrocytes and is important for neuronal function. Its biosynthesis is severely reduced in mouse models of Huntington's disease. One possible mechanism is a diminished nuclear translocation of the transcription factor sterol regulatory element binding protein 2 (SREBP2) and, consequently, reduced activation of SREBP-controlled genes in the cholesterol biosynthesis pathway. Read More

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Astroglial Cx30 differentially impacts synaptic activity from hippocampal principal cells and interneurons.

Glia 2021 May 11. Epub 2021 May 11.

Neuroglial Interactions in Cerebral Physiopathology, Center for Interdisciplinary Research in Biology (CIRB), Collège de France, Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche UMR 7241, Institut National de la Santé et de la Recherche Médicale (INSERM) U1050, Labex Memolife, PSL-Research University, Paris, France.

Astrocytes play important roles in brain function via dynamic structural and functional interactions with neurons. Yet the underlying mechanisms remain poorly defined. A typical feature of astrocytes is the high expression of connexins, which mediate their extensive intercellular communication and regulate their structural properties. Read More

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The Pathological Role of Astrocytic MAOB in Parkinsonism Revealed by Genetic Ablation and Over-expression of MAOB.

Exp Neurobiol 2021 Apr;30(2):113-119

Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.

The cause of Parkinson's disease has been traditionally believed to be the dopaminergic neuronal death in the substantia nigra pars compacta (SNpc). This traditional view has been recently challenged by the proposal that reactive astrocytes serve as key players in the pathology of Parkinson's disease through excessive GABA release. This aberrant astrocytic GABA is synthesized by the enzymatic action of monoamine oxidase B (MAOB), whose pharmacological inhibition and gene-silencing are reported to significantly alleviate parkinsonian motor symptoms in animal models of Parkinson's disease. Read More

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Pen-2 negatively regulates the differentiation of oligodendrocyte precursor cells into astrocytes in the central nervous system.

J Neurosci 2021 May 7. Epub 2021 May 7.

State Key Laboratory of Pharmaceutical Biotechnology, MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing University, 12 Xuefu Avenue, Nanjing, Jiangsu Province, China, 210061.

Mutations on γ-secretase subunits are associated with neurological diseases. Whereas the role of γ-secretase in neurogenesis has been intensively studied, little is known about its role in astrogliogenesis. Recent evidence has demonstrated that astrocytes can be generated from oligodendrocyte (OL) precursor cells (OPCs). Read More

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Activation of spinal dorsal horn astrocytes by noxious stimuli involves descending noradrenergic signaling.

Mol Brain 2021 May 10;14(1):79. Epub 2021 May 10.

Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.

Astrocytes are critical regulators of neuronal function in the central nervous system (CNS). We have previously shown that astrocytes in the spinal dorsal horn (SDH) have increased intracellular Ca levels following intraplantar injection of the noxious irritant, formalin. However, the underlying mechanisms remain unknown. Read More

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IL-9-triggered lncRNA Gm13568 regulates Notch1 in astrocytes through interaction with CBP/P300: contribute to the pathogenesis of experimental autoimmune encephalomyelitis.

J Neuroinflammation 2021 May 11;18(1):108. Epub 2021 May 11.

Xuzhou Key Laboratory of Neurobiology, Department of Neurobiology and Anatomy, Xuzhou Medical University, Xuzhou, Jiangsu, 221004, People's Republic of China.

Background: Interleukin 9 (IL-9), produced mainly by T helper 9 (Th9) cells, has been recognized as an important regulator in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Astrocytes respond to IL-9 and reactive astrocytes always associate with blood-brain barrier damage, immune cell infiltration, and spinal injury in MS and EAE. Several long non-coding RNAs (lncRNAs) with aberrant expression have been identified in the pathogenesis of MS. Read More

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Mild hypothermia facilitates mitochondrial transfer from astrocytes to injured neurons during oxygen-glucose deprivation/reoxygenation.

Neurosci Lett 2021 May 7:135940. Epub 2021 May 7.

Department of Anesthesiology, Second Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, China. Electronic address:

Mitochondrial dysfunction is now considered an important sign of neuronal death during cerebral ischemia/reperfusion (I/R) injury. Studies have shown that the transfer of mitochondria from astrocytes to injured neurons contributes to endogenous neuroprotection after stroke. Basic and clinical studies have shown that mild hypothermia exerts a clear protective effect on neurons after cerebral ischemic injury, but the role of mild hypothermia in this endogenous neuroprotective mechanism remains unclear. Read More

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Growing role of S100B protein as a putative therapeutic target for neurological -and nonneurological- disorders.

Neurosci Biobehav Rev 2021 May 7. Epub 2021 May 7.

Department of Translational Medicine and Surgery, Section of General Pathology, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy; Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo Agostino Gemelli 1-8, 00168 Rome, Italy. Electronic address:

S100B is a calcium-binding protein mainly expressed by astrocytes, but also localized in other definite neural and extra-neural cell types. While its presence in biological fluids is widely recognized as a reliable biomarker of active injury, growing evidence now indicates that high levels of S100B are suggestive of pathogenic processes in different neural, but also extra-neural, disorders. Indeed, modulation of S100B levels correlates with the occurrence of clinical and/or toxic parameters in experimental models of diseases such as Alzheimer's and Parkinson's diseases, amyotrophic lateral sclerosis, muscular dystrophy, multiple sclerosis, acute neural injury, inflammatory bowel disease, uveal and retinal disorders, obesity, diabetes and cancer, thus directly linking the levels of S100B to pathogenic mechanisms. Read More

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Astrocyte and glutamate involvement in the pathogenesis of epilepsy in Alzheimer's disease.

Epilepsia 2021 May 10. Epub 2021 May 10.

Department of Neuroscience, Central Clinical School, The Alfred Hospital, Monash University, Melbourne, Vic., Australia.

Alzheimer's disease (AD) can increase the risk of epilepsy by up to 10-fold compared to healthy age-matched controls. However, the pathological mechanisms that underlie this increased risk are poorly understood. Because disruption in brain glutamate homeostasis has been implicated in both AD and epilepsy, this might play a mechanistic role in the pathogenesis of epilepsy in AD. Read More

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A role for the immune system-released activating agent (ISRAA) in the ontogenetic development of brain astrocytes.

PLoS One 2021 10;16(5):e0248455. Epub 2021 May 10.

Department of Molecular Medicine, College of Medicine and Medical Sciences, Princess Al Jawhara Center for Molecular Medicine, Genetics and Inherited Diseases, Arabian Gulf University, Manama, Bahrain.

The Immune System-Released Activating Agent (ISRAA) was discovered as a novel molecule that functions as a mediator between the nervous and immune systems in response to a nervous stimulus following an immune challenge. This research investigated the role of ISRAA) in promoting the ontogeny of the mouse brain astrocytes. Astrocyte cultures were prepared from two-month-old BALB/c mice. Read More

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The emerging role of FTY720 as a sphingosine 1-phosphate analog for the treatment of ischemic stroke: The cellular and molecular mechanisms.

Brain Behav 2021 May 10:e02179. Epub 2021 May 10.

Histomorphometry and Stereology Research Centre, Shiraz University of Medical Sciences, Shiraz, Iran.

Finding novel and effective drugs for the treatment of ischemic stroke is warranted because there is not a definitive treatment for this prevalent disease. Due to the relevance between the sphingosine 1-phosphate (S1P) receptor and several neurological diseases including ischemic stroke, it seems that fingolimod (FTY720), as an agonist of S1P receptor, can be a useful therapeutic strategy in these patients. FTY720 is the first oral drug approved by the US food and drug administration for the treatment of multiple sclerosis. Read More

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Targeted Thrombospondin-1 Expression in Ocular Vascular Development and Neovascularization.

Front Cell Dev Biol 2021 21;9:671989. Epub 2021 Apr 21.

McPherson Eye Research Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States.

Tight regulation of positive and negative regulators of angiogenesis is essential, particularly in the eye where their dysregulation can lead to vision loss. Thrombospondin-1 (TSP1) is a matricellular protein that negatively regulates angiogenesis and inflammation in the eye. It aids ocular vascular homeostasis such that its loss contributes to increased retinal vascular density and pathologic ocular neovascularization. Read More

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Recovery of Depleted miR-146a in ALS Cortical Astrocytes Reverts Cell Aberrancies and Prevents Paracrine Pathogenicity on Microglia and Motor Neurons.

Front Cell Dev Biol 2021 23;9:634355. Epub 2021 Apr 23.

Instituto de Investigação do Medicamento (iMed.ULisboa), Faculdade de Farmácia, Universidade de Lisboa, Lisbon, Portugal.

Reactive astrocytes in Amyotrophic Lateral Sclerosis (ALS) change their molecular expression pattern and release toxic factors that contribute to neurodegeneration and microglial activation. We and others identified a dysregulated inflammatory miRNA profile in ALS patients and in mice models suggesting that they represent potential targets for therapeutic intervention. Such cellular miRNAs are known to be released into the secretome and to be carried by small extracellular vesicles (sEVs), which may be harmful to recipient cells. Read More

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Dendritic cells lower the permeability of endothelial monolayers.

Cell Mol Bioeng 2012 Jun 4;5(2):184-193. Epub 2012 Feb 4.

Department of Bioengineering, Imperial College London.

The permeability of cultured endothelial monolayers is higher than the permeability of endothelium . Co-culture with astrocytes can induce a tight, blood-brain-barrier phenotype in aortic endothelium . We hypothesised that dendritic cells, which reside in the intima of non-cerebral arteries and have features in common with astrocytes, may also reduce the permeability of cultured aortic endothelium. Read More

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Capturing T Lymphocytes' Dynamic Interactions With Human Neural Cells Using Time-Lapse Microscopy.

Front Immunol 2021 22;12:668483. Epub 2021 Apr 22.

Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montreal, QC, Canada.

To fully perform their functions, T lymphocytes migrate within organs' parenchyma and interact with local cells. Infiltration of T lymphocytes within the central nervous system (CNS) is associated with numerous neurodegenerative disorders. Nevertheless, how these immune cells communicate and respond to neural cells remains unresolved. Read More

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Editorial: Synaptic Loss and Neurodegeneration.

Front Cell Neurosci 2021 21;15:681029. Epub 2021 Apr 21.

Axe Neurosciences, Centre de Recherche du CHU de Québec, Université Laval, Québec City, QC, Canada.

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Canavan Disease as a Model for Gene Therapy-Mediated Myelin Repair.

Front Cell Neurosci 2021 23;15:661928. Epub 2021 Apr 23.

Horae Gene Therapy Center, University of Massachusetts Medical School, Worcester, MA, United States.

In recent years, the scientific and therapeutic fields for rare, genetic central nervous system (CNS) diseases such as leukodystrophies, or white matter disorders, have expanded significantly in part due to technological advancements in cellular and clinical screenings as well as remedial therapies using novel techniques such as gene therapy. However, treatments aimed at normalizing the pathological changes associated with leukodystrophies have especially been complicated due to the innate and variable effects of glial abnormalities, which can cause large-scale functional deficits in developmental myelination and thus lead to downstream neuronal impairment. Emerging research in the past two decades have depicted glial cells, particularly oligodendrocytes and astrocytes, as key, regulatory modulators in constructing and maintaining myelin function and neuronal viability. Read More

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Pathogenic Functions of Tumor Necrosis Factor Receptor- Factor 6 Signaling Traumatic Brain Injury.

Front Mol Neurosci 2021 21;14:629910. Epub 2021 Apr 21.

Department of Rehabilitation Medicine, Affiliated Hospital of Nantong University, Nantong, China.

Neuroinflammation contributes to delayed (secondary) neurodegeneration following traumatic brain injury (TBI). Tumor necrosis factor receptor-associated factor 6 (TRAF6) signaling may promote post-TBI neuroinflammation, thereby exacerbating secondary injury. This study investigated the pathogenic functions of TRAF6 signaling following TBI and . Read More

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Physical Exercise: A Versatile Anti-Inflammatory Tool Involved in the Control of Hypothalamic Satiety Signaling.

Exerc Immunol Rev 2021 ;27:7-23

Laboratory of Molecular Biology of Exercise, University of Campinas (UNICAMP), Limeira, São Paulo, Brazil.

The hypothalamus plays a critical role in the control of food consumption and energy expenditure. Fatty diets can elicit an inflammatory response in specific hypothalamic cells, including astrocytes, tanycytes, and microglia, disrupting anorexigenic signals in region-specific hypothalamic neurons, contributing to overeating and body weight gain. In this study, we present an update regarding the knowledge of the effects of physical exercise on inflammatory signaling and circuits to control hunger in the hypothalamus in obesity conditions. Read More

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January 2021

Progress in Elucidating Pathophysiology of Mucolipidosis IV.

Neurosci Lett 2021 May 6:135944. Epub 2021 May 6.

Center for Genomic Medicine and Department of Neurology, Massachusetts General Hospital Research Institute and Harvard Medical School, Boston, MA, 02114, United States. Electronic address:

Mucolipidosis IV (MLIV) is an autosomal-recessive disease caused by loss-of-function mutations in the MCOLN1 gene encoding the non-selective cationic lysosomal channel transient receptor potential mucolipin-1 (TRPML1). Patients with MLIV suffer from severe motor and cognitive deficits that manifest in early infancy and progressive loss of vision leading to blindness in the second decade of life. There are no therapies available for MLIV and the unmet medical need is extremely high. Read More

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Ethanol inhibition of lateral orbitofrontal cortex neuron excitability is mediated via dopamine D1/D5 receptor-induced release of astrocytic glycine.

Neuropharmacology 2021 May 6:108600. Epub 2021 May 6.

Department of Neuroscience, Addiction Sciences Division Medical University of South Carolina Charleston, SC 29425; Department of Psychiatry and Behavioral Sciences, Addiction Sciences Division Medical University of South Carolina Charleston, SC 29425. Electronic address:

Recent findings from this laboratory demonstrate that ethanol reduces the intrinsic excitability of orbitofrontal cortex (OFC) neurons via activation of strychnine-sensitive glycine receptors. Although the mechanism linking ethanol to the release of glycine is currently unknown, astrocytes are a source of neurotransmitters including glycine and activation of dopamine D1-like receptors has been reported to enhance extracellular levels of glycine via a functional reversal of the astrocytic glycine transporter GlyT1. We recently reported that like ethanol, dopamine or a D1/D5 receptor agonist increases a tonic current in lateral OFC (lOFC) neurons. Read More

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White matter abnormalities and iron deposition in prenatal mucolipidosis IV- fetal imaging and pathology.

Metab Brain Dis 2021 May 8. Epub 2021 May 8.

Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.

Mucolipidosis type IV (MLIV; OMIM 252,650) is an autosomal recessive lysosomal disorder caused by mutations in MCOLN1. MLIV causes psychomotor impairment and progressive vision loss. The major hallmarks of postnatal brain MRI are hypomyelination and thin corpus callosum. Read More

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Organic Cation Transporter Expression and Function in the CNS.

Authors:
Douglas H Sweet

Handb Exp Pharmacol 2021 May 8. Epub 2021 May 8.

Department of Pharmaceutics, School of Pharmacy, Virginia Commonwealth University, Richmond, VA, USA.

The blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB) represent major control checkpoints protecting the CNS, by exerting selective control over the movement of organic cations and anions into and out of the CNS compartment. In addition, multiple CNS cell types, e.g. Read More

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Loss of liver X receptor β in astrocytes leads to anxiety-like behaviors via regulating synaptic transmission in the medial prefrontal cortex in mice.

Mol Psychiatry 2021 May 7. Epub 2021 May 7.

Department of Developmental Neuropsychology, School of Psychology, Third Military Medical University (Army Medical University), Chongqing, PR China.

Astrocytes are integral components of synaptic transmission, and their dysfunction leads to neuropsychiatric disorders such as anxiety and depression. Liver X receptor β (LXRβ) is expressed in astrocytes, and LXRβ global knockout mice shows impaired synaptic formation. In order to define the role of LXRβ in astrocytes, we used a conditional Cre-loxP system to specifically remove LXRβ from astrocytes. Read More

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Methylation as a key regulator of Tau aggregation and neuronal health in Alzheimer's disease.

Cell Commun Signal 2021 May 7;19(1):51. Epub 2021 May 7.

Neurobiology Group, Division of Biochemical Sciences, CSIR-National Chemical Laboratory (CSIR-NCL), Dr. Homi Bhabha Road, 411008,, Pune, India.

Neurodegenerative diseases like Alzheimer's, Parkinson's and Huntington's disease involves abnormal aggregation and accumulation of toxic proteins aggregates. Post-translational modifications (PTMs) of the causative proteins play an important role in the etiology of disease as they could either slow down or accelerate the disease progression. Alzheimer disease is associated with the aggregation and accumulation of two major protein aggregates-intracellular neurofibrillary tangles made up of microtubule-associated protein Tau and extracellular Amyloid-β plaques. Read More

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Neurovascular-modulation: A review of primary vascular responses to transcranial electrical stimulation as a mechanism of action.

Brain Stimul 2021 May 4. Epub 2021 May 4.

Department of Biomedical Engineering, The City College of New York (CCNY), New York, NY, USA.

Background: The ubiquitous vascular response to transcranial electrical stimulation (tES) has been attributed to the secondary effect of neuronal activity forming the classic neurovascular coupling. However, the current density delivered transcranially concentrates in: A) the cerebrospinal fluid of subarachnoid space where cerebral vasculature resides after reaching the dural and pial surfaces and B) across the blood-brain-barrier after reaching the brain parenchyma. Therefore, it is anticipated that tES has a primary vascular influence. Read More

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A survey of the mouse hindbrain in the fed and fasted state using single-nucleus RNA sequencing.

Mol Metab 2021 May 4:101240. Epub 2021 May 4.

MRC Metabolic Diseases Unit, University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, UK. Electronic address:

Objective: The area postrema (AP) and the nucleus tractus solitaris (NTS), located in the hindbrain, are key nuclei that sense and integrate peripheral nutritional signals and, consequently, regulate feeding behaviour. While single cell transcriptomics have been used in mice to reveal the gene expression profile and heterogeneity of key hypothalamic populations, similar in-depth studies have not yet been performed in the hindbrain.

Methods: Using single-nucleus RNA sequencing, we provide a detailed survey of 16,034 cells within the AP and NTS of the mouse, in the fed and fasted state. Read More

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Stimulation of astrocytic sigma-1 receptor is sufficient to ameliorate inflammation- induced depression.

Behav Brain Res 2021 May 4;410:113344. Epub 2021 May 4.

Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Jiangsu, China. Electronic address:

Astrocytes play important roles in the development of depression. As a promising target for antidepressant development, sigma-1 receptor (Sig-1R) is reported to promote activation of astrocyte in chronic stress-induced depression in our previous study. However, astrocytes are hyper-activated in inflammation-induced depression, raising concerns of whether stimulation of astrocytic Sig-1R would exert antidepressant-like effect in inflammation-induced depression. Read More

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Genetic mosaicism, intrafamilial phenotypic heterogeneity, and molecular defects of a novel missense SLC6A1 mutation associated with epilepsy and ADHD.

Exp Neurol 2021 May 5;342:113723. Epub 2021 May 5.

Department of Neurology, Vanderbilt University Medical Center, Nashville, TN, 37232, United States of America. Electronic address:

Background: Mutations in SLC6A1, encoding γ-aminobutyric acid (GABA) transporter 1 (GAT-1), have been recently associated with a spectrum of neurodevelopmental disorders ranging from variable epilepsy syndromes, intellectual disability (ID), autism and others. To date, most identified mutations are de novo. We here report a pedigree of two siblings associated with myoclonic astatic epilepsy, attention deficit hyperactivity disorder (ADHD), and ID. Read More

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