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https://www.readbyqxmd.com/read/27914807/phosphorylation-of-p53-by-lrrk2-induces-microglial-tumor-necrosis-factor-%C3%AE-mediated-neurotoxicity
#1
Dong Hwan Ho, Wongi Seol, Jin Hwan Eun, Il-Hong Son
Leucine-rich repeat kinase (LRRK2), a major causal gene of Parkinson's disease (PD), functions as a kinase. The most prevalent mutation of LRRK2 is G2019S. It exhibits increased kinase activity compared to the wildtype LRRK2. Previous studies have shown that LRRK2 can phosphorylate p53 at T304 and T377 of threonine-X-arginine (TXR) motif in neurons. Reduction of LRRK2 expression or inhibition of LRRK2 kinase activity has been shown to be able to alleviate LPS-induced neuroinflammation in microglia cells. In this study, we found that LRRK2 could also phosphorylate p53 in microglia model BV2 cells...
November 30, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27912057/gut-microbiota-regulate-motor-deficits-and-neuroinflammation-in-a-model-of-parkinson-s-disease
#2
Timothy R Sampson, Justine W Debelius, Taren Thron, Stefan Janssen, Gauri G Shastri, Zehra Esra Ilhan, Collin Challis, Catherine E Schretter, Sandra Rocha, Viviana Gradinaru, Marie-Francoise Chesselet, Ali Keshavarzian, Kathleen M Shannon, Rosa Krajmalnik-Brown, Pernilla Wittung-Stafshede, Rob Knight, Sarkis K Mazmanian
The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. However, a functional link between gut bacteria and neurodegenerative diseases remains unexplored. Synucleinopathies are characterized by aggregation of the protein α-synuclein (αSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease (PD). Using mice that overexpress αSyn, we report herein that gut microbiota are required for motor deficits, microglia activation, and αSyn pathology...
December 1, 2016: Cell
https://www.readbyqxmd.com/read/27889907/activation-of-nur77-in-microglia-attenuates-proinflammatory-mediators-production-and-protects-dopaminergic-neurons-from-inflammation-induced-cell-death
#3
Tian-Ya Liu, Xiao-Ying Yang, Long-Tai Zheng, Guang-Hui Wang, Xue-Chu Zhen
Microglia-mediated neuroinflammation plays a critical role in the pathological development of Parkinson's disease (PD). Orphan nuclear receptor Nur77 (Nur77) is abundant in neurons, while its role in microglia-mediated neuroinflammation remains unclear. The present data demonstrated that the expression of Nur77 in microglia was reduced accompanied with microglia activation in response to lipopolysaccharide (LPS) in vitro and in experimental MPTP-PD mouse model. Nur77 overexpression or application of Nur77 agonist CsnB suppressed the expression of proinflammatory genes, such as iNOS, COX-2, IL-1β, and TNF-α in the activated microglia, while silenced Nur77 exaggerated the inflammatory responses in microglia...
November 27, 2016: Journal of Neurochemistry
https://www.readbyqxmd.com/read/27859864/l-dopa-induced-dyskinesia-and-neuroinflammation-do-microglia-and-astrocytes-play-a-role
#4
Anna R Carta, Giovanna Mulas, Mariza Bortolanza, Terence Duarte, Elisabetta Pillai, Gilberto Fisone, Rita Vozari Raisman, Elaine Del Bel
In Parkinson's disease (PD), L-DOPA therapy leads to the emergence of motor complications including L-DOPA-induced dyskinesia (LID). LID relies on a sequence of pre- and postsynaptic neuronal events, leading to abnormal corticostriatal neurotransmission and maladaptive changes in striatal projection neurons. In recent years, additional non-neuronal mechanisms have been proposed to contribute to LID. Among these mechanisms considerable attention has been focused on L-DOPA-induced inflammatory responses. Microglia and astrocytes are the main actors in neuroinflammatory responses, and their double role at the interface between immune and neurophysiological responses is starting to be elucidated...
November 17, 2016: European Journal of Neuroscience
https://www.readbyqxmd.com/read/27808010/role-of-neuroinflammation-and-latent-transcription-factors-in-pathogenesis-of-parkinson-s-disease
#5
Rishi Pal, Prafulla Chandra Tiwari, Rajendra Nath, Kamlesh Kumar Pant
Parkinson's disease (PD) the second most common age-associated progressive neurodegenerative disorder is characterized by loss of dopaminergic neurons, cytoplasmic inclusions of aggregated proteins (Lewy bodies), and neuroinflammation. The inflammation of neurons causes release of various inflammatory mediators (IFNs, EGF, IL5, IL6, HGF, LIF and BMP2). The hallmarks of neuroinflammation are the presence of activated microglia and reactive astrocytes in the parenchyma of the CNS and increased production of cytokines, chemokines, prostaglandins, complement cascade proteins, and reactive oxygen and nitrogen species (ROS/RNS) which in some cases can result in disruption of the blood brain barrier and direct participation of the adaptive immune system...
November 3, 2016: Neurological Research
https://www.readbyqxmd.com/read/27790086/traumatic-brain-injury-leads-to-development-of-parkinson-s-disease-related-pathology-in-mice
#6
Daniela Impellizzeri, Michela Campolo, Giuseppe Bruschetta, Rosalia Crupi, Marika Cordaro, Irene Paterniti, Salvatore Cuzzocrea, Emanuela Esposito
Traumatic brain injury (TBI) is a major health and socio-economic problem that affects all societies. This condition results from the application of external physical strength to the brain that leads to transitory or permanent structural and functional impairments. Moreover, TBI is a risk factor for neurodegeneration and can e.g., increase the risk for Parkinson's disease (PD), a late-onset neurodegenerative disorder with loss of dopaminergic neurons in substantia nigra. In this study, we wanted to explore the possible development of PD-related pathology within the context of an experimental model of TBI...
2016: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/27769915/clk1-deficiency-promotes-neuroinflammation-and-subsequent-dopaminergic-cell-death-through-regulation-of-microglial-metabolic-reprogramming
#7
Ruinan Gu, Fali Zhang, Gang Chen, Chaojun Han, Jay Liu, Zhaoxiang Ren, Yi Zhu, John L Waddington, Long Tai Zheng, Xuechu Zhen
Clock (Clk)1/COQ7 is a mitochondrial hydroxylase that is necessary for the biosynthesis of ubiquinone (coenzyme Q or UQ). Here, we investigate the role of Clk1 in neuroinflammation and consequentially dopaminergic (DA) neuron survival. Reduced expression of Clk1 in microglia enhanced the LPS-induced proinflammatory response and promoted aerobic glycolysis. Inhibition of glycolysis abolished Clk1 deficiency-induced hypersensitivity to the inflammatory stimulation. Mechanistic studies demonstrated that mTOR/HIF-1α and ROS/HIF-1α signaling pathways were involved in Clk1 deficiency-induced aerobic glycolysis...
October 18, 2016: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/27742410/baicalein-attenuates-%C3%AE-synuclein-aggregation-inflammasome-activation-and-autophagy-in-the-mpp-treated-nigrostriatal-dopaminergic-system-in-vivo
#8
Kai-Chih Hung, Hui-Ju Huang, Yi-Ting Wang, Anya Maan-Yuh Lin
ETHNOPHARMACOLOGICAL RELEVANCE: Neuroinflammation, oxidative stress, and protein aggregation form a vicious cycle in the pathophysiology of Parkinson's disease (PD); activated microglia is the main location of neuroinflammation. A Chinese medicine book, "Shanghan Lun", known as the "Treatises on Cold damage Diseases" has suggested that Scutellaria baicalensis Georgi is effective in treating CNS diseases. The anti-inflammatory mechanisms of baicalein, a phenolic flavonoid in the dried root of Scutellaria baicalensis Georgi, remain to be explored...
October 11, 2016: Journal of Ethnopharmacology
https://www.readbyqxmd.com/read/27736702/polymer-brain-nanotherapeutics-for-multipronged-inhibition-of-microglial-%C3%AE-synuclein-aggregation-activation-and-neurotoxicity
#9
Neal K Bennett, Rebecca Chmielowski, Dalia S Abdelhamid, Jonathan J Faig, Nicola Francis, Jean Baum, Zhiping P Pang, Kathryn E Uhrich, Prabhas V Moghe
Neuroinflammation, a common neuropathologic feature of neurodegenerative disorders including Parkinson disease (PD), is frequently exacerbated by microglial activation. The extracellular protein α-synuclein (ASYN), whose aggregation is characteristic of PD, remains a key therapeutic target, but the control of synuclein trafficking and aggregation within microglia has been challenging. First, we established that microglial internalization of monomeric ASYN was mediated by scavenger receptors (SR), CD36 and SRA1, and was rapidly accompanied by the formation of ASYN oligomers...
December 2016: Biomaterials
https://www.readbyqxmd.com/read/27713030/role-of-the-jak-stat-signaling-pathway-in-regulation-of-innate-immunity-in-neuroinflammatory-diseases
#10
Zhaoqi Yan, Sara A Gibson, Jessica A Buckley, Hongwei Qin, Etty N Benveniste
The Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) signaling pathway is utilized by numerous cytokines and interferons, and is essential for the development and function of both innate and adaptive immunity. Aberrant activation of the JAK/STAT pathway is evident in neuroinflammatory diseases such as Multiple Sclerosis and Parkinson's Disease. Innate immunity is the front line defender of the immune system and is composed of various cell types, including microglia, macrophages and neutrophils...
October 3, 2016: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/27708561/protective-microglia-and-their-regulation-in-parkinson-s-disease
#11
Weidong Le, Junjiao Wu, Yu Tang
Microglia-mediated neuroinflammation is a hallmark of Parkinson's disease (PD). In the brains of patients with PD, microglia have both neurotoxic and neuroprotective effects, depending on their activation state. In this review, we focus on recent research demonstrating the neuroprotective role of microglia in PD. Accumulating evidence indicates that the protective mechanisms of microglia may result from their regulation of transrepression pathways via nuclear receptors, anti-inflammatory responses, neuron-microglia crosstalk, histone modification, and microRNA regulation...
2016: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/27697481/differential-induction-of-dyskinesia-and-neuroinflammation-by-pulsatile-versus-continuous-l-dopa-delivery-in-the-6-ohda-model-of-parkinson-s-disease
#12
Giovanna Mulas, Elena Espa, Sandro Fenu, Saturnino Spiga, Giovanni Cossu, Elisabetta Pillai, Ezio Carboni, Gabriella Simbula, Dragana Jadžić, Fabrizio Angius, Stefano Spolitu, Barbara Batetta, Daniela Lecca, Andrea Giuffrida, Anna R Carta
Neuroinflammation is associated with l-DOPA treatment in Parkinson's disease (PD), suggesting a role in l-DOPA-induced dyskinesia (LID), however it is unclear whether increased inflammation is specifically related to the dyskinetic outcome of l-DOPA treatment. Diversely from oral l-DOPA, continuous intrajejunal l-DOPA infusion is associated with very low dyskinetic outcome in PD patients. We reproduced these regimens of administration in 6-OHDA-lesioned hemiparkinsonian rats, where dyskinetic responses and striatal neuroinflammation induced by chronic pulsatile (DOPAp) or continuous (DOPAc) l-DOPA were compared...
December 2016: Experimental Neurology
https://www.readbyqxmd.com/read/27693549/pharmacologic-antagonism-of-dopamine-receptor-d3-attenuates-neurodegeneration-and-motor-impairment-in-a-mouse-model-of-parkinson-s-disease
#13
Daniela Elgueta, María S Aymerich, Francisco Contreras, Andro Montoya, Marta Celorrio, Estefanía Rojo-Bustamante, Eduardo Riquelme, Hugo González, Mónica Vásquez, Rafael Franco, Rodrigo Pacheco
Neuroinflammation involves the activation of glial cells, which is associated to the progression of neurodegeneration in Parkinson's disease. Recently, we and other researchers demonstrated that dopamine receptor D3 (D3R)-deficient mice are completely refractory to neuroinflammation and consequent neurodegeneration associated to the acute intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In this study we examined the therapeutic potential and underlying mechanism of a D3R-selective antagonist, PG01037, in mice intoxicated with a chronic regime of administration of MPTP and probenecid (MPTPp)...
September 28, 2016: Neuropharmacology
https://www.readbyqxmd.com/read/27666480/alpha-synuclein-activates-bv2-microglia-dependent-on-its-aggregation-state
#14
Alana Hoffmann, Benjamin Ettle, Ariane Bruno, Anna Kulinich, Anna-Carin Hoffmann, Julia von Wittgenstein, Jürgen Winkler, Wei Xiang, Johannes C M Schlachetzki
Synucleinopathies such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA) are defined by the presence of intracellular alpha-synuclein aggregates in neurons and/or oligodendrocytes. In addition, post mortem tissue analysis revealed profound changes in microglial morphology, indicating microglial activation and neuroinflammation. Thus, alpha-synuclein may directly activate microglia, leading to increased production of key pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β), which in turn modulates the disease progression...
October 28, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27637804/chronic-mild-stress-accelerates-the-progression-of-parkinson-s-disease-in-a53t-%C3%AE-synuclein-transgenic-mice
#15
Qimei Wu, Xiaoyu Yang, Yu Zhang, Lei Zhang, Linyin Feng
Daily stress is associated with increased risk for various diseases, and numerous studies have provided evidence that environmental stress leads to deleterious effects on the central nervous system. However, it remains unclear whether chronic stress exacerbates the progression of Parkinson's disease (PD). To investigate this hypothesis, we determined the effect of chronic mild stress (CMS) on the pathogenesis of PD in a transgenic mice line that overexpresses the human A53T mutant α-synuclein (A53T Tg mice)...
November 2016: Experimental Neurology
https://www.readbyqxmd.com/read/27622765/alpha-synuclein-proteins-promote-pro-inflammatory-cascades-in-microglia-stronger-effects-of-the-a53t-mutant
#16
Claire Hoenen, Audrey Gustin, Cindy Birck, Mélanie Kirchmeyer, Nicolas Beaume, Paul Felten, Luc Grandbarbe, Paul Heuschling, Tony Heurtaux
Parkinson's disease (PD) is histologically described by the deposition of α-synuclein, whose accumulation in Lewy bodies causes dopaminergic neuronal death. Although most of PD cases are sporadic, point mutations of the gene encoding the α-synuclein protein cause inherited forms of PD. There are currently six known point mutations that result in familial PD. Oxidative stress and neuroinflammation have also been described as early events associated with dopaminergic neuronal degeneration in PD. Though it is known that microglia are activated by wild-type α-synuclein, little is known about its mutated forms and the signaling cascades responsible for this microglial activation...
2016: PloS One
https://www.readbyqxmd.com/read/27618286/l-dopa-induced-dyskinesia-in-parkinson-s-disease-are-neuroinflammation-and-astrocytes-key-elements
#17
Elaine Del-Bel, Mariza Bortolanza, Maurício Dos-Santos-Pereira, Keila Bariotto, Rita Raisman-Vozari
Inflammation in Parkinson's disease (PD) is a new concept that has gained ground due to the potential of mitigating dopaminergic neuron death by decreasing inflammation. The solution to this question is likely to be complex. We propose here that the significance of inflammation in PD may go beyond the nigral cell death. The pathological process that underlies PD requires years to reach its full extent. A growing body of evidence has been accumulated on the presence of multiple inflammatory signs in the brain of PD patients even in very late stages of the disease...
December 2016: Synapse
https://www.readbyqxmd.com/read/27574481/prothrombin-kringle-2-a-potential-inflammatory-pathogen-in-the-parkinsonian-dopaminergic-system
#18
REVIEW
Eunju Leem, Kyoung Hoon Jeong, So-Yoon Won, Won-Ho Shin, Sang Ryong Kim
Although accumulating evidence suggests that microglia-mediated neuroinflammation may be crucial for the initiation and progression of Parkinson's disease (PD), and that the control of neuroinflammation may be a useful strategy for preventing the degeneration of nigrostriatal dopaminergic (DA) projections in the adult brain, it is still unclear what kinds of endogenous biomolecules initiate microglial activation, consequently resulting in neurodegeneration. Recently, we reported that the increase in the levels of prothrombin kringle-2 (pKr-2), which is a domain of prothrombin that is generated by active thrombin, can lead to disruption of the nigrostriatal DA projection...
August 2016: Experimental Neurobiology
https://www.readbyqxmd.com/read/27555548/transient-glutathione-depletion-in-the-substantia-nigra-compacta-is-associated-with-neuroinflammation-in-rats
#19
Mei-Li Díaz-Hung, Arianna Yglesias-Rivera, Luis Fernando Hernández-Zimbrón, Sandra Orozco-Suárez, Jenny Laura Ruiz-Fuentes, Alexis Díaz-García, Rilda León-Martínez, Lisette Blanco-Lezcano, Nancy Pavón-Fuentes, Lourdes Lorigados-Pedre
Glutathione (GSH) deficiency has been identified as an early event in the progression of Parkinson's disease. However, the role of GSH in the etiology and pathogenesis of this neurodegenerative disorder is not well established. The aim of this study is to assess the effect of transient GSH depletion in the substantia nigra pars compacta (SNpc) on neuroinflammation after the injection of a single dose of l-buthionine sulfoximine (BSO) into the SNpc of male Sprague-Dawley rats. The results showed that BSO treatment stimulates microglia (p<0...
October 29, 2016: Neuroscience
https://www.readbyqxmd.com/read/27549180/neuroprotective-effect-of-nerolidol-against-neuroinflammation-and-oxidative-stress-induced-by-rotenone
#20
Hayate Javed, Sheikh Azimullah, Salema B Abul Khair, Shreesh Ojha, M Emdadul Haque
BACKGROUND: Parkinson disease (PD) is a movement disorder affecting 1 % of people over the age of 60. The etiology of the disease is unknown; however, accumulating evidence suggests that mitochondrial defects, oxidative stress, and neuroinflammation play important roles in developing the disease. Current medications for PD can only improve its symptoms, but are unable to halt its progressive nature. Although many therapeutic approaches are available, new drugs are urgently needed for the treatment of PD...
2016: BMC Neuroscience
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