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https://www.readbyqxmd.com/read/28550263/microglial-and-neuronal-tdp-43-pathology-in-anti-iglon5-related-tauopathy
#1
Annachiara Cagnin, Sara Mariotto, Michele Fiorini, Marina Gaule, Nicola Bonetto, Matteo Tagliapietra, Emanuele Buratti, Gianluigi Zanusso, Sergio Ferrari, Salvatore Monaco
A novel neuronal tauopathy, mainly confined to hypothalamus and brainstem tegmentum, has recently been reported in patients with autoantibodies to the neuronal cell-adhesion molecule IgLON5. We describe a patient with anti-IgLON5 syndrome, who presented with dysautonomia and sleep disorder, followed by subacute dementia. Postmortem brain examination disclosed neuronal tau pathology prevailing in the hippocampus, amygdala, and locus coeruleus, in addition to microglial/neuronal TDP-43 pathology, with overexpression of aberrantly phosphorylated forms and neurotoxic truncated fragments, in basal ganglia, nucleus basalis, thalamus, and midbrain...
May 26, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28549481/late-onset-alzheimer-s-disease-genetics-implicates-microglial-pathways-in-disease-risk
#2
REVIEW
Anastasia G Efthymiou, Alison M Goate
Alzheimer's disease (AD) is a highly heritable complex disease with no current effective prevention or treatment. The majority of drugs developed for AD focus on the amyloid cascade hypothesis, which implicates Aß plaques as a causal factor in the disease. However, it is possible that other underexplored disease-associated pathways may be more fruitful targets for drug development. Findings from gene network analyses implicate immune networks as being enriched in AD; many of the genes in these networks fall within genomic regions that contain common and rare variants that are associated with increased risk of developing AD...
May 26, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28546318/an-environment-dependent-transcriptional-network-specifies-human-microglia-identity
#3
David Gosselin, Dylan Skola, Nicole G Coufal, Inge R Holtman, Johannes C M Schlachetzki, Eniko Sajti, Baptiste N Jaeger, Carolyn O'Connor, Conor Fitzpatrick, Martina P Pasillas, Monique Pena, Amy Adair, David G Gonda, Michael L Levy, Richard M Ransohoff, Fred H Gage, Christopher K Glass
Microglia play essential roles in central nervous system (CNS) homeostasis and influence diverse aspects of neuronal function. However, the transcriptional mechanisms that specify human microglia phenotypes are largely unknown. We examined the transcriptomes and epigenetic landscapes of human microglia isolated from surgically resected brain tissue ex vivo and following transition to an in vitro environment. Transfer to a tissue culture environment results in rapid and extensive downregulation of microglia-specific genes that are induced in primitive mouse macrophages following migration into the fetal brain...
May 25, 2017: Science
https://www.readbyqxmd.com/read/28546058/the-role-of-il-6-in-neurodevelopment-after-prenatal-stress
#4
Serena B Gumusoglu, Rebecca S Fine, Samuel J Murray, Jada L Bittle, Hanna E Stevens
Prenatal stress exposure is associated with adverse psychiatric outcomes, including autism and ADHD, as well as locomotor and social inhibition and anxiety-like behaviors in animal offspring. Similarly, maternal immune activation also contributes to psychiatric risk and aberrant offspring behavior. The mechanisms underlying these outcomes are not clear. Offspring microglia and the pro-inflammatory cytokine interleukin-6 (IL-6), known to influence microglia, may serve as common mechanisms between prenatal stress and prenatal immune activation...
May 22, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28545778/current-pharmacological-developments-in-2-3-4-5-tetrahydroxystilbene-2-o-%C3%AE-d-glucoside-tsg
#5
REVIEW
Jingjing Wu, Wenfeng Hu, Yu Gong, Peng Wang, Lijuan Tong, Xiangfan Chen, Zhuo Chen, Xiaole Xu, Wenjuan Yao, Wei Zhang, Chao Huang
2,3,4',5-tetrahydroxystilbene 2-O-β-D-glucoside (TSG), a resveratrol analog with glucoside, is purified from a traditional Chinese herbal medicine polygonum multiflorum. It has been extensively studied in last decade and known to exert strong anti-inflammatory, anti-oxidative, anti-apoptotic, and free radical scavenging activities, and therefore has been listed as a potential agent for disease therapies. Recent studies extend well-beyond effects of TSG on the injury of neurons, cardiomyocytes and endothelial cells, and report important functions of TSG in a lot of pathophysiological conditions...
May 22, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28545543/inhibition-of-colony-stimulating-factor-1-receptor-early-in-disease-ameliorates-motor-deficits-in-sca1-mice
#6
Wenhui Qu, Andrea Johnson, Joo Hyun Kim, Abigail Lukowicz, Daniel Svedberg, Marija Cvetanovic
BACKGROUND: Polyglutamine (polyQ) expansion in the protein Ataxin-1 (ATXN1) causes spinocerebellar ataxia type 1 (SCA1), a fatal dominantly inherited neurodegenerative disease characterized by motor deficits, cerebellar neurodegeneration, and gliosis. Currently, there are no treatments available to delay or ameliorate SCA1. We have examined the effect of depleting microglia during the early stage of disease by using PLX, an inhibitor of colony-stimulating factor 1 receptor (CSFR1), on disease severity in a mouse model of SCA1...
May 25, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28545141/prion-pathogenesis-is-unaltered-in-the-absence-of-sirp%C3%AE-mediated-don-t-eat-me-signaling
#7
Mario Nuvolone, Marta Paolucci, Silvia Sorce, Veronika Kana, Rita Moos, Takashi Matozaki, Adriano Aguzzi
Prion diseases are neurodegenerative conditions caused by misfolding of the prion protein, leading to conspicuous neuronal loss and intense microgliosis. Recent experimental evidence point towards a protective role of microglia against prion-induced neurodegeneration, possibly through elimination of prion-containing apoptotic bodies. The molecular mechanisms by which microglia recognize and eliminate apoptotic cells in the context of prion diseases are poorly defined. Here we investigated the possible involvement of signal regulatory protein α (SIRPα), a key modulator of host cell phagocytosis; SIRPα is encoded by the Sirpa gene that is genetically linked to the prion gene Prnp...
2017: PloS One
https://www.readbyqxmd.com/read/28544775/potentiation-of-spinal-glutamatergic-response-in-the-neuron-glia-interactions-underlies-the-intrathecal-il-1%C3%AE-induced-thermal-hyperalgesia-in-rats
#8
Chun-Sung Sung, Zhi-Hong Wen, Chien-Wei Feng, Chun-Hong Chen, Shi-Ying Huang, Nan-Fu Chen, Wu-Fu Chen, Chih-Shung Wong
AIMS: We previously demonstrated that intrathecal IL-1β upregulated phosphorylation of p38 mitogen-activated protein kinase (P-p38 MAPK) and inducible nitric oxide synthase (iNOS) in microglia and astrocytes in spinal cord, increased nitric oxide (NO) release into cerebrospinal fluid, and induced thermal hyperalgesia in rats. This study investigated the role of spinal glutamatergic response in intrathecal IL-1β-induced nociception in rats. METHODS: The pretreatment effects of MK-801 (5 μg), minocycline (20 μg), and SB203580 (5 μg) on intrathecal IL-1β (100 ng) in rats were measured by behavior, Western blotting, CSF analysis, and immunofluorescence studies...
May 19, 2017: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/28544365/anti-aging-drugs-reduce-hypothalamic-inflammation-in-a-sex-specific-manner
#9
Marianna Sadagurski, Gillian Cady, Richard A Miller
Aging leads to hypothalamic inflammation, but does so more slowly in mice whose lifespan has been extended by mutations that affect GH/IGF-1 signals. Early-life exposure to GH by injection, or to nutrient restriction in the first 3 weeks of life, also modulate both lifespan and the pace of hypothalamic inflammation. Three drugs extend lifespan of UM-HET3 mice in a sex-specific way: acarbose (ACA), 17-α-estradiol (17αE2), and nordihydroguaiaretic acid (NDGA), with more dramatic longevity increases in males in each case...
May 20, 2017: Aging Cell
https://www.readbyqxmd.com/read/28543680/downregulation-of-mir-7116-5p-in-microglia-by-mpp-sensitizes-tnf-%C3%AE-production-to-induce-dopaminergic-neuron-damage
#10
Qian He, Qing Wang, Chao Yuan, Yizheng Wang
Activation of microglia resulting in exacerbated inflammation expression plays an important role in degeneration of dopaminergic (DA) neurons in the pathogenesis of Parkinson's disease (PD). However, how this enhanced inflammation is induced in microglia remains largely unclear. Here, in the mouse PD model induced by 1-methyl-4-phenyl-1,2,3,6-tetra hydropyridine (MPTP), we found that miR-7116-5p in microglia has a crucial role in this inflammation. 1-methyl-4-phenylpyridinium (MPP(+) ) is uptaken by microglia through organic cation transporter 3 (OCT3) to downregulate miR-7116-5p, an miRNA found to target tumor necrosis factor alpha (TNF-α)...
May 22, 2017: Glia
https://www.readbyqxmd.com/read/28542572/arachidonic-acid-containing-phosphatidylcholine-increases-due-to-microglial-activation-in-ipsilateral-spinal-dorsal-horn-following-spared-sciatic-nerve-injury
#11
Tomohiro Banno, Takao Omura, Noritaka Masaki, Hideyuki Arima, Dongmin Xu, Ayako Okamoto, Michael Costigan, Alban Latremoliere, Yukihiro Matsuyama, Mitsutoshi Setou
Peripheral nerve injury induces substantial molecular changes in the somatosensory system that leads to maladaptive plasticity and cause neuropathic pain. Understanding the molecular pathways responsible for the development of neuropathic pain is essential to the development of novel rationally designed therapeutics. Although lipids make up to half of the dry weight of the spinal cord, their relation with the development of neuropathic pain is poorly understood. We aimed to elucidate the regulation of spinal lipids in response to neuropathic peripheral nerve injury in mice by utilizing matrix-assisted laser desorption/ionization imaging mass spectrometry, which allows visualization of lipid distribution within the cord...
2017: PloS One
https://www.readbyqxmd.com/read/28542400/intracellular-ca2-homeostasis-and-jak1-stat3-pathway-are-involved-in-the-protective-effect-of-propofol-on-bv2-microglia-against-hypoxia-induced-inflammation-and-apoptosis
#12
Yan Lu, Yuechao Gu, Xiaowei Ding, Jiaqiang Wang, Jiawei Chen, Changhong Miao
BACKGROUND: Perioperative hypoxia may induce microglial inflammation and apoptosis, resulting in brain injury. The neuroprotective effect of propofol against hypoxia has been reported, but the underlying mechanisms are far from clear. In this study, we explored whether and how propofol could attenuate microglia BV2 cells from CoCl2-induced hypoxic injury. METHODS: Mouse microglia BV2 cells were pretreated with propofol, and then stimulated with CoCl2. TNF-α level in the culture medium was measured by ELISA kit...
2017: PloS One
https://www.readbyqxmd.com/read/28542295/therapeutic-benefits-of-phosphodiesterase-4b-inhibition-after-traumatic-brain-injury
#13
Nicole M Wilson, Mark E Gurney, W Dalton Dietrich, Coleen M Atkins
Traumatic brain injury (TBI) initiates a deleterious inflammatory response that exacerbates pathology and worsens outcome. This inflammatory response is partially mediated by a reduction in cAMP and a concomitant upregulation of cAMP-hydrolyzing phosphodiesterases (PDEs) acutely after TBI. The PDE4B subfamily, specifically PDE4B2, has been found to regulate cAMP in inflammatory cells, such as neutrophils, macrophages and microglia. To determine if PDE4B regulates inflammation and subsequent pathology after TBI, adult male Sprague Dawley rats received sham surgery or moderate parasagittal fluid-percussion brain injury (2 ± 0...
2017: PloS One
https://www.readbyqxmd.com/read/28541408/loss-of-homeostatic-microglia-and-patterns-of-their-activation-in-active-multiple-sclerosis
#14
Tobias Zrzavy, Simon Hametner, Isabella Wimmer, Oleg Butovsky, Howard L Weiner, Hans Lassmann
Microglia and macrophages accumulate at the sites of active demyelination and neurodegeneration in the multiple sclerosis brain and are thought to play a central role in the disease process. We used recently described markers to characterize the origin and functional states of microglia/macrophages in acute, relapsing and progressive multiple sclerosis. We found microglia activation in normal white matter of controls and that the degree of activation increased with age. This microglia activation was more pronounced in the normal-appearing white matter of patients in comparison to controls and increased with disease duration...
May 24, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28540665/different-molecular-mechanisms-mediate-direct-or-glia-dependent-prion-protein-fragment-90-231-neurotoxic-effects-in-cerebellar-granule-neurons
#15
Stefano Thellung, Elena Gatta, Francesca Pellistri, Valentina Villa, Alessandro Corsaro, Mario Nizzari, Mauro Robello, Tullio Florio
Glia over-stimulation associates with amyloid deposition contributing to the progression of central nervous system neurodegenerative disorders. Here we analyze the molecular mechanisms mediating microglia-dependent neurotoxicity induced by prion protein (PrP)90-231, an amyloidogenic polypeptide corresponding to the protease-resistant portion of the pathological prion protein scrapie (PrP(Sc)). PrP90-231 neurotoxicity is enhanced by the presence of microglia within neuronal culture, and associated to a rapid neuronal [Ca(++)] i increase...
May 25, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28540600/microglial-interferon-signaling-and-white-matter
#16
Ashley McDonough, Richard V Lee, Jonathan R Weinstein
Microglia, the resident immune cells of the CNS, are primary regulators of the neuroimmune response to injury. Type I interferons (IFNs), including the IFNαs and IFNβ, are key cytokines in the innate immune system. Their activity is implicated in the regulation of microglial function both during development and in response to neuroinflammation, ischemia, and neurodegeneration. Data from numerous studies in multiple sclerosis (MS) and stroke suggest that type I IFNs can modulate the microglial phenotype, influence the overall neuroimmune milieu, regulate phagocytosis, and affect blood-brain barrier integrity...
May 25, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28540131/parkinson-s-disease-microglial-macrophage-induced-immunoexcitotoxicity-as-a-central-mechanism-of-neurodegeneration
#17
REVIEW
Russell L Blaylock
Parkinson's disease is one of the several neurodegenerative disorders that affects aging individuals, with approximately 1% of those over the age of 60 years developing the disorder in their lifetime. The disease has the characteristics of a progressive disorder in most people, with a common pattern of pathological change occurring in the nervous system that extends beyond the classical striatal degeneration of dopaminergic neurons. Earlier studies concluded that the disease was a disorder of alpha-synuclein, with the formation of aggregates of abnormal alpha-synuclein being characteristic...
2017: Surgical Neurology International
https://www.readbyqxmd.com/read/28539882/function-and-dysfunction-of-microglia-during-brain-development-consequences-for-synapses-and-neural-circuits
#18
REVIEW
Rosa C Paolicelli, Maria T Ferretti
Many diverse factors, ranging from stress to infections, can perturb brain homeostasis and alter the physiological activity of microglia, the immune cells of the central nervous system. Microglia play critical roles in the process of synaptic maturation and brain wiring during development. Any perturbation affecting microglial physiological function during critical developmental periods could result in defective maturation of synaptic circuits. In this review, we critically appraise the recent literature on the alterations of microglial activity induced by environmental and genetic factors occurring at pre- and early post-natal stages...
2017: Frontiers in Synaptic Neuroscience
https://www.readbyqxmd.com/read/28539419/microglia-are-irrelevant-for-neuronal-degeneration-and-axon-regeneration-after-acute-injury
#19
Alexander M Hilla, Heike Diekmann, Dietmar Fischer
The role of microglia in de- and regenerative processes after damage of the nervous system still remains ambiguous, partially due to the paucity of appropriate investigative methods. Here, we show that treatment with the pharmacological colony stimulating factor 1 receptor inhibitor PLX5622 specifically eliminated microglia in murine retinae and optic nerves. Interestingly, time course and extent of retinal ganglion cell (RGC) degeneration after optic nerve crush remained unaffected upon microglia depletion, although remnants of pre-labeled apoptotic RGCs were not cleared from the retina in these animals...
May 24, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28539349/sleep-loss-promotes-astrocytic-phagocytosis-and-microglial-activation-in-mouse-cerebral-cortex
#20
Michele Bellesi, Luisa de Vivo, Mattia Chini, Francesca Gilli, Giulio Tononi, Chiara Cirelli
We previously found that Mertk and its ligand Gas6, astrocytic genes involved in phagocytosis, are upregulated after acute sleep deprivation. These results suggested that astrocytes may engage in phagocytic activity during extended wake, but direct evidence was lacking. Studies in humans and rodents also found that sleep loss increases peripheral markers of inflammation, but whether these changes are associated with neuroinflammation and/or activation of microglia, the brain's resident innate immune cells, was unknown...
May 24, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
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