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https://www.readbyqxmd.com/read/29054466/astrocyte-reactivity-and-astrogliosis-after-spinal-cord-injury
#1
REVIEW
Seiji Okada, Masamitsu Hara, Kazu Kobayakawa, Yoshihiro Matsumoto, Yasuharu Nakashima
After traumatic injuries of the central nervous system (CNS), including spinal cord injury (SCI), astrocytes surrounding the lesion become reactive and typically undergo hypertrophy and process extension. These reactive astrocytes migrate centripetally to the lesion epicenter and aid in the tissue repair process, however, they eventually become scar-forming astrocytes and form a glial scar which produces axonal growth inhibitors and prevents axonal regeneration. This sequential phenotypic change has long been considered to be unidirectional and irreversible; thus glial scarring is one of the main causes of the limited regenerative capability of the CNS...
October 17, 2017: Neuroscience Research
https://www.readbyqxmd.com/read/29053032/a-mouse-model-of-subcortical-vascular-dementia-reflecting-degeneration-of-cerebral-white-matter-and-microcirculation
#2
Eek-Sung Lee, Jin-Hui Yoon, Jiye Choi, Faris R Andika, Taekwan Lee, Yong Jeong
Subcortical vascular dementia(SVaD) is associated with white matter damage, lacunar infarction, and degeneration of cerebral microcirculation. Currently available mouse models can mimic only partial aspects of human SVaD features. Here, we combined bilateral common carotid artery stenosis (BCAS) with a hyperlipidaemia model in order to develop a mouse model of SVaD; 10- to 12-week-old apolipoprotein E (ApoE)-deficient or wild-type C57BL/6J mice were subjected to sham operation or chronic cerebral hypoperfusion with BCAS using micro-coils...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/29050399/diagnostic-criteria-for-chronic-lymphocytic-inflammation-with-pontine-perivascular-enhancement-responsive-to-steroids-clippers
#3
W Oliver Tobin, Yong Guo, Karl N Krecke, Joseph E Parisi, Claudia F Lucchinetti, Sean J Pittock, Jay Mandrekar, Divyanshu Dubey, Jan Debruyne, B Mark Keegan
Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is a central nervous system inflammatory syndrome predominantly affecting the brainstem, cerebellum, and spinal cord. Following its initial description, the salient features of CLIPPERS have been confirmed and expanded upon, but the lack of formalized diagnostic criteria has led to reports of patients with dissimilar features purported to have CLIPPERS. We evaluated clinical, radiological and pathological features of patients referred for suspected CLIPPERS and propose diagnostic criteria to discriminate CLIPPERS from non-CLIPPERS aetiologies...
September 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29050386/brain-monoamine-oxidase-b-and-a-in-human-parkinsonian-dopamine-deficiency-disorders
#4
Junchao Tong, Gausiha Rathitharan, Jeffrey H Meyer, Yoshiaki Furukawa, Lee-Cyn Ang, Isabelle Boileau, Mark Guttman, Oleh Hornykiewicz, Stephen J Kish
See Jellinger (doi:10.1093/awx190) for a scientific commentary on this article. The enzyme monoamine oxidases (B and A subtypes, encoded by MAOB and MAOA, respectively) are drug targets in the treatment of Parkinson's disease. Inhibitors of MAOB are used clinically in Parkinson's disease for symptomatic purposes whereas the potential disease-modifying effect of monoamine oxidase inhibitors is debated. As astroglial cells express high levels of MAOB, the enzyme has been proposed as a brain imaging marker of astrogliosis, a cellular process possibly involved in Parkinson's disease pathogenesis as elevation of MAOB in astrocytes might be harmful...
September 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29046125/pretreatment-with-n-acetyl-cysteine-suppresses-chronic-reactive-astrogliosis-following-maternal-nanoparticle-exposure-during-gestational-period
#5
Atsuto Onoda, Ken Takeda, Masakazu Umezawa
Early pregnant employees are potentially and unintendedly exposed to industrial chemicals including nanoparticles. Developmental toxicity of nanoparticle exposure has been concerned because exposure to fine particle including carbon black nanoparticle (CB-NP) during the brain developmental stage enhances the risk of brain disorders. Maternal CB-NP exposure dose-dependently induces astrogliosis, which is an abnormal increase in the reactive astrocytes with glial fibrillary acidic protein (GFAP) and aquaporin-4 overexpression due to the destruction of nearby neurons and blood vessels...
October 19, 2017: Nanotoxicology
https://www.readbyqxmd.com/read/29044639/inflammatory-pathology-markers-activated-microglia-and-reactive-astrocytes-in-early-and-late-onset-alzheimer-disease-a-post-mortem-study
#6
Ricardo Taipa, Vitor Ferreira, Paulo Brochado, Andrew Robinson, Inês Reis, Fernanda Marques, David M Mann, Manuel Melo Pires, Nuno Sousa
AIMS: The association between the pathological features of AD and dementia is stronger in younger old persons than in older old persons suggesting that additional factors are involved in the clinical expression of dementia in the oldest old. Cumulative data suggests that neuroinflammation plays a prominent role in Alzheimer's disease (AD) and different studies reported an age-associated dysregulation of the neuroimmune system. Consequently, we sought to characterize the pattern of microglial cell activation and astrogliosis in brain post-mortem tissue of pathologically confirmed cases of early and late onset AD (EOAD and LOAD) and determine their relation to age...
October 17, 2017: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/29039346/astrogliosis-has-different-dynamics-after-cell-transplantation-and-mechanical-impact-in-the-rodent-model-of-parkinson-s-disease
#7
Nikola Tomov, Lachezar Surchev, Clemens Wiedenmann, Máté Daniel Döbrössy, Guido Nikkhah
BACKGROUND: Transplantation of fetal mesencephalic tissue is a well-established concept for functional reinnervation of the dopamine-depleted rat striatum. However, no extensive description of the glial reaction of the host brain following this procedure has been carried out. AIMS: The present study aims at a quantitative and qualitative analysis of the astrogliosis surrounding intrastriatal grafts and comparing it to the reaction caused by a mechanical injury with the transplantation instrument only...
October 17, 2017: Balkan Medical Journal
https://www.readbyqxmd.com/read/29037246/effectors-of-th1-and-th17-cells-act-on-astrocytes-and-augment-their-neuroinflammatory-properties
#8
Chittappen K Prajeeth, Julius Kronisch, Reza Khorooshi, Benjamin Knier, Henrik Toft-Hansen, Viktoria Gudi, Stefan Floess, Jochen Huehn, Trevor Owens, Thomas Korn, Martin Stangel
BACKGROUND: Autoreactive Th1 and Th17 cells are believed to mediate the pathology of multiple sclerosis in the central nervous system (CNS). Their interaction with microglia and astrocytes in the CNS is crucial for the regulation of the neuroinflammation. Previously, we have shown that only Th1 but not Th17 effectors activate microglia. However, it is not clear which cells are targets of Th17 effectors in the CNS. METHODS: To understand the effects driven by Th17 cells in the CNS, we induced experimental autoimmune encephalomyelitis in wild-type mice and CD4(+) T cell-specific integrin α4-deficient mice where trafficking of Th1 cells into the CNS was affected...
October 16, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29037241/the-potassium-channel-kca3-1-constitutes-a-pharmacological-target-for-astrogliosis-associated-with-ischemia-stroke
#9
Mengni Yi, Tianjiao Wei, Yanxia Wang, Qin Lu, Gaoxian Chen, Xiaoling Gao, Herbert M Geller, Hongzhuan Chen, Zhihua Yu
BACKGROUND: Reactive astrogliosis is one of the significantly pathological features in ischemic stroke accompanied with changes in gene expression, morphology, and proliferation. KCa3.1 was involved in TGF-β-induced astrogliosis in vitro and also contributed to astrogliosis-mediated neuroinflammation in neurodegeneration disease. METHODS: Wild type mice and KCa3.1(-/-) mice were subjected to permanent middle cerebral artery occlusion (pMCAO) to evaluate the infarct areas by 2,3,5-triphenyltetrazolium hydrochloride staining and neurological deficit...
October 16, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29033188/ppp1cc-is-associated-with-astrocyte-and-microglia-proliferation-after-traumatic-spinal-cord-injury-in-rats
#10
Xiaojuan Liu, Shen Huang, Chun Liu, Xia Liu, Yuntian Shen, Zhiming Cui
Reactive astrogliosis and microgliosis after spinal cord injury (SCI) contribute to glial scar formation that impedes axonal regeneration. The mechanisms underlying reactive astrocyte and microglia proliferation upon injury remain partially understood. Protein phosphatase 1, catalytic subunit, gamma isozyme (PPP1CC) participates in cell proliferation, differentiation and apoptosis. However, the expression and functions of PPP1CC following SCI are still unknown. In this study, an acute spinal cord contusion injury model in adult rats was established to investigate the potential role of PPP1CC during the pathological process of SCI...
September 28, 2017: Pathology, Research and Practice
https://www.readbyqxmd.com/read/29023667/postnatal-reduction-of-tuberous-sclerosis-complex-1-expression-in-astrocytes-and-neurons-causes-seizures-in-an-age-dependent-manner
#11
Jia Zou, Bo Zhang, David H Gutmann, Michael Wong
OBJECTIVE: Epilepsy is one of the most prominent symptoms of tuberous sclerosis complex (TSC), a genetic disorder, and may be related to developmental defects resulting from impaired TSC1 or TSC2 gene function in astrocytes and neurons. Inactivation of the Tsc1 gene driven by a glial-fibrillary acidic protein (GFAP) promoter during embryonic brain development leads to widespread pathologic effects on astrocytes and neurons, culminating in severe, progressive epilepsy in mice (Tsc1(GFAP)(-Cre) mice)...
October 12, 2017: Epilepsia
https://www.readbyqxmd.com/read/29021835/progressive-changes-in-hippocampal-cytoarchitecture-in-a-neurodevelopmental-rat-model-of-epilepsy-implications-for-understanding-presymptomatic-epileptogenesis-predictive-diagnosis-and-targeted-treatments
#12
Paul B Bernard, Leslie A Ramsay, Debra S MacDonald, R Andrew Tasker
Epilepsies affect about 4% of the population and are frequently characterized by a prolonged "silent" period before the onset of spontaneous seizures. Most current animal models of epilepsy either involve acute seizure induction or kindling protocols that induce repetitive seizures. We have developed a rat model of epilepsy that is characterized by a slowly progressing series of behavioral abnormalities prior to the onset of behavioral seizures. In the current study, we further describe an accompanying progression of cytoarchitectural changes in the hippocampal formation...
September 2017: EPMA Journal
https://www.readbyqxmd.com/read/28989099/astroglial-correlates-of-neuropsychiatric-disease-from-astrocytopathy-to-astrogliosis
#13
REVIEW
Ronald Kim, Kati L Healey, Marian T Sepulveda-Orengo, Kathryn J Reissner
Complex roles for astrocytes in health and disease continue to emerge, highlighting this class of cells as integral to function and dysfunction of the nervous system. In particular, escalating evidence strongly implicates a range of changes in astrocyte structure and function associated with neuropsychiatric diseases including major depressive disorder, schizophrenia, and addiction. These changes can range from astrocytopathy, degeneration, and loss of function, to astrogliosis and hypertrophy, and can be either adaptive or maladaptive...
October 5, 2017: Progress in Neuro-psychopharmacology & Biological Psychiatry
https://www.readbyqxmd.com/read/28987175/inflammatory-demyelinating-diseases-of-the-central-nervous-system
#14
Romana Höftberger, Hans Lassmann
Inflammatory demyelinating diseases are a heterogeneous group of disorders, which occur against the background of an acute or chronic inflammatory process. The pathologic hallmark of multiple sclerosis (MS) is the presence of focal demyelinated lesions with partial axonal preservation and reactive astrogliosis. Demyelinated plaques are present in the white as well as gray matter, such as the cerebral or cerebellar cortex and brainstem nuclei. Activity of the disease process is reflected by the presence of lesions with ongoing myelin destruction...
2017: Handbook of Clinical Neurology
https://www.readbyqxmd.com/read/28987165/mitochondrial-diseases
#15
Maria J Molnar, Gabor G Kovacs
Mitochondrial disorders represent a major challenge in medicine. Most of the mitochondrial proteins are encoded by the nuclear DNA (nDNA), whereas a very small fraction is encoded by the mitochondrial DNA (mtDNA). Mutations in mtDNA or mitochondria-related nDNA genes can result in mitochondrial dysfunction. The disease usually affects multiple organs in varying locations and severity; however, there are some forms which affect a single organ. The diagnosis of mitochondrial disorders is based on clinical examination, biochemical and histopathologic examinations, functional studies, and molecular genetic testing...
2017: Handbook of Clinical Neurology
https://www.readbyqxmd.com/read/28984618/reduced-th-expression-and-%C3%AE-synuclein-accumulation-contribute-towards-nigrostriatal-dysfunction-in-experimental-hepatic-encephalopathy
#16
Isabel Suárez, Guillermo Bodega, Miguel Rubio, Benjamín Fernández
PURPOSE: The present work examines α-synuclein expression in the nigrostriatal system of a rat chronic hepatic encephalopathy model induced by portacaval anastomosis (PCA). There is evidence that dopaminergic dysfunction in disease conditions is strongly associated with such expression. Possible relationships among dopaminergic neurons, astroglial cells and α-synuclein expression were sought. METHODS: Brain tissue samples from rats at 1 and 6 months post-PCA, and controls, were analysed immunohistochemically using antibodies against tyrosine hydroxylase (TH), α-synuclein, glial fibrillary acidic protein (GFAP) and ubiquitin (Ub)...
2017: Restorative Neurology and Neuroscience
https://www.readbyqxmd.com/read/28974375/murine-sialidase-neu3-facilitates-gm2-degradation-and-bypass-in-mouse-model-of-tay-sachs-disease
#17
Volkan Seyrantepe, Secil Akyildiz Demir, Zehra Kevser Timur, Johanna Von Gerichten, Christian Marsching, Esra Erdemli, Emin Oztas, Kohta Takahashi, Kazunori Yamaguchi, Nurselin Ates, Buket Dönmez Demir, Turgay Dalkara, Katrin Erich, Carsten Hopf, Roger Sandhoff, Taeko Miyagi
Tay-Sachs disease is a severe lysosomal storage disorder caused by mutations in Hexa, the gene that encodes for the α subunit of lysosomal β-hexosaminidase A (HEXA), which converts GM2 to GM3 ganglioside. Unexpectedly, Hexa(-/-) mice have a normal lifespan and show no obvious neurological impairment until at least one year of age. These mice catabolize stored GM2 ganglioside using sialidase(s) to remove sialic acid and form the glycolipid GA2, which is further processed by β-hexosaminidase B. Therefore, the presence of the sialidase (s) allows the consequences of the Hexa defect to be bypassed...
September 30, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28971314/alterations-of-brain-energy-metabolism-in-type-2-diabetic-goto-kakizaki-rats-measured-in-vivo-by-13-c-magnetic-resonance-spectroscopy
#18
Freya-Merret Girault, Sarah Sonnay, Rolf Gruetter, João M N Duarte
Type 2 diabetes (T2D) is associated with deterioration of brain structure and function. Here, we tested the hypothesis that T2D induces a reorganization of the brain metabolic networks that support brain function. For that, alterations of neuronal and glial energy metabolism were investigated in a T2D model, the Goto-Kakizaki (GK) rat. (13)C magnetic resonance spectroscopy in vivo at 14.1 T was used to detect (13)C labeling incorporation into carbons of glutamate, glutamine, and aspartate in the brain of GK (n = 7) and Wistar (n = 13) rats during intravenous [1,6-(13)C]glucose administration...
October 2, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28960838/increased-adult-neurogenesis-associated-with-reactive-astrocytosis-occurs-prior-to-neuron-loss-in-a-mouse-model-of-neurodegenerative-disease
#19
Ting-Ting Liu, Xiao-Lian Ye, Jin-Ping Zhang, Ting-Ting Yu, Shan-Shan Cheng, Xiao-Chuan Zou, Yun Xu, Gui-Quan Chen, Zhen-Yu Yin
AIMS: This study was to investigate whether cell proliferation and adult neurogenesis are affected at early neurodegenerative stage when neuron loss has not begun to display. METHODS AND RESULTS: Forebrain-specific nicastrin (NCT) conditional knockout (cKO) mice were generated by crossing NCT(f/f) with CaMKIIα-Cre Tg mice. BrdU was used as a lineage tracer to label proliferating neural progenitor cells (NPCs). Immunohistochemistry (IHC) on BrdU indicated that the total number of BrdU positive (+) cells was increased in NCT cKO mice...
September 27, 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/28958576/guanidinylated-neomycin-conjugation-enhances-intranasal-enzyme-replacement-in-the-brain
#20
Wenyong Tong, Chrissa A Dwyer, Bryan E Thacker, Charles A Glass, Jillian R Brown, Kristina Hamil, Kelley W Moremen, Stéphane Sarrazin, Philip L S M Gordts, Lara E Dozier, Gentry N Patrick, Yitzhak Tor, Jeffrey D Esko
Iduronidase (IDUA)-deficient mice accumulate glycosaminoglycans in cells and tissues and exhibit many of the same neuropathological symptoms of patients suffering from Mucopolysaccharidosis I. Intravenous enzyme-replacement therapy for Mucopolysaccharidosis I ameliorates glycosaminoglycan storage and many of the somatic aspects of the disease but fails to treat neurological symptoms due to poor transport across the blood-brain barrier. In this study, we examined the delivery of IDUA conjugated to guanidinoneomycin (GNeo), a molecular transporter...
August 12, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
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