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https://www.readbyqxmd.com/read/29892066/block-of-a1-astrocyte-conversion-by-microglia-is-neuroprotective-in-models-of-parkinson-s-disease
#1
Seung Pil Yun, Tae-In Kam, Nikhil Panicker, SangMin Kim, Yumin Oh, Jong-Sung Park, Seung-Hwan Kwon, Yong Joo Park, Senthilkumar S Karuppagounder, Hyejin Park, Sangjune Kim, Nayeon Oh, Nayoung Alice Kim, Saebom Lee, Saurav Brahmachari, Xiaobo Mao, Jun Hee Lee, Manoj Kumar, Daniel An, Sung-Ung Kang, Yunjong Lee, Kang Choon Lee, Dong Hee Na, Donghoon Kim, Sang Hun Lee, Viktor V Roschke, Shane A Liddelow, Zoltan Mari, Ben A Barres, Valina L Dawson, Seulki Lee, Ted M Dawson, Han Seok Ko
Activation of microglia by classical inflammatory mediators can convert astrocytes into a neurotoxic A1 phenotype in a variety of neurological diseases1,2 . Development of agents that could inhibit the formation of A1 reactive astrocytes could be used to treat these diseases for which there are no disease-modifying therapies. Glucagon-like peptide-1 receptor (GLP1R) agonists have been indicated as potential neuroprotective agents for neurologic disorders such as Alzheimer's disease and Parkinson's disease3-13 ...
June 11, 2018: Nature Medicine
https://www.readbyqxmd.com/read/29850876/immunohistochemical-and-molecular-investigations-show-alteration-in-the-inflammatory-profile-of-multiple-system-atrophy-brain
#2
Aoife P Kiely, Christina E Murray, Sandrine C Foti, Bridget C Benson, Robert Courtney, Catherine Strand, Tammaryn Lashley, Janice L Holton
Multiple system atrophy (MSA) is an adult-onset neurodegenerative disease characterized by aggregation of α-synuclein in oligodendrocytes to form glial cytoplasmic inclusions. According to the distribution of neurodegeneration, MSA is subtyped as striatonigral degeneration (SND), olivopontocerebellar atrophy (OPCA), or as combination of these 2 (mixed MSA). In the current study, we aimed to investigate regional microglial populations and gene expression in the 3 different MSA subtypes. Microscopy with microglial marker Iba-1 combined with either proinflammatory marker CD68 or anti-inflammatory marker Arginase-1 was analyzed in control, SND, and OPCA cases (n = 5) using paraffin embedded sections...
April 23, 2018: Journal of Neuropathology and Experimental Neurology
https://www.readbyqxmd.com/read/29780321/toll-like-receptor-2-signaling-and-current-approaches-for-therapeutic-modulation-in-synucleinopathies
#3
REVIEW
Ian F Caplan, Kathleen A Maguire-Zeiss
The innate immune response in the central nervous system (CNS) is implicated as both beneficial and detrimental to health. Integral to this process are microglia, the resident immune cells of the CNS. Microglia express a wide variety of pattern-recognition receptors, such as Toll-like receptors, that detect changes in the neural environment. The activation of microglia and the subsequent proinflammatory response has become increasingly relevant to synucleinopathies, including Parkinson's disease the second most prevalent neurodegenerative disease...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29779267/%C3%AE-synuclein-activates-innate-immunity-but-suppresses-interferon-%C3%AE-expression-in-murine-astrocytes
#4
Jintang Wang, Zheng Chen, Jeremy Walston, Peisong Gao, Maolong Gao, Sean X Leng
Glial activation and neuroinflammation contribute to pathogenesis of neurodegenerative diseases, linked to neuron loss and dysfunction. α-Synuclein (α-syn), as a metabolite of neuron, can induce microglia activation to trigger innate immune response. However, whether α-syn, as well as its mutants (A53T, A30P and E46K), induces astrocyte activation and inflammatory response is not fully elucidated. In this study, we used A53T mutant and wildtype α-syns to stimulate primary astrocytes in dose- and time-dependent manners (0...
May 19, 2018: European Journal of Neuroscience
https://www.readbyqxmd.com/read/29775624/characterization-and-comparative-analysis-of-a-new-mouse-microglial-cell-model-for-studying-neuroinflammatory-mechanisms-during-neurotoxic-insults
#5
Souvarish Sarkar, Emir Malovic, Deeksha Sarda, Vivek Lawana, Dharmin Rokad, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy, Anumantha G Kanthasamy
Microglia are the first responders of the central nervous system, acting as the key modulators of neuroinflammation observed during neurotoxic insults as well as in the pathophysiology of several neurodegenerative disorders including Alzheimer's (AD), Parkinson's (PD), and Huntington's diseases (HD). The number of publications on microglia has increased steadily throughout the past decade because of immense interests in the neuroinflammation that precedes the neurodegenerative process. To study microglial biology and its role in modulating neuroinflammation, immortalized microglial cell lines derived from mice, rats, and humans have been developed...
May 15, 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29770111/chronic-caffeine-treatment-protects-against-%C3%AE-synucleinopathy-by-reestablishing-autophagy-activity-in-the-mouse-striatum
#6
Yanan Luan, Xiangpeng Ren, Wu Zheng, Zhenhai Zeng, Yingzi Guo, Zhidong Hou, Wei Guo, Xingjun Chen, Fei Li, Jiang-Fan Chen
Despite converging epidemiological evidence for the inverse relationship of regular caffeine consumption and risk of developing Parkinson's disease (PD) with animal studies demonstrating protective effect of caffeine in various neurotoxin models of PD, whether caffeine can protect against mutant α-synuclein (α-Syn) A53T-induced neurotoxicity in intact animals has not been examined. Here, we determined the effect of chronic caffeine treatment using the α-Syn fibril model of PD by intra-striatal injection of preformed A53T α-Syn fibrils...
2018: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/29755323/environmental-enrichment-prevents-transcriptional-disturbances-induced-by-alpha-synuclein-overexpression
#7
Zinah Wassouf, Thomas Hentrich, Sebastian Samer, Carola Rotermund, Philipp J Kahle, Ingrid Ehrlich, Olaf Riess, Nicolas Casadei, Julia M Schulze-Hentrich
Onset and progression of neurodegenerative disorders, including synucleinopathies such as Parkinson's disease, have been associated with various environmental factors. A highly compelling association from a therapeutic point of view has been found between a physically active lifestyle and a significantly reduced risk for Parkinson's disease. Mimicking such conditions in animal models by promoting physical activity, social interactions, and novel surroundings yields in a so-called enriched environment known to enhance adult neurogenesis, increase synaptic plasticity, and decelerate neuronal loss...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29755317/microglial-phagocytosis-and-its-regulation-a-therapeutic-target-in-parkinson-s-disease
#8
REVIEW
Elzbieta Janda, Laura Boi, Anna R Carta
The role of phagocytosis in the neuroprotective function of microglia has been appreciated for a long time, but only more recently a dysregulation of this process has been recognized in Parkinson's disease (PD). Indeed, microglia play several critical roles in central nervous system (CNS), such as clearance of dying neurons and pathogens as well as immunomodulation, and to fulfill these complex tasks they engage distinct phenotypes. Regulation of phenotypic plasticity and phagocytosis in microglia can be impaired by defects in molecular machinery regulating critical homeostatic mechanisms, including autophagy...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29747690/a53t-%C3%AE-synuclein-overexpression-in-murine-locus-coeruleus-induces-parkinson-s-disease-like-pathology-in-neurons-and-glia
#9
Martin Timo Henrich, Fanni Fruzsina Geibl, Bolam Lee, Wei-Hua Chiu, James Benjamin Koprich, Jonathan Michael Brotchie, Lars Timmermann, Niels Decher, Lina Anita Matschke, Wolfgang Hermann Oertel
Degeneration of noradrenergic locus coeruleus neurons occurs during the prodromal phase of Parkinson's disease and contributes to a variety of non-motor symptoms, e.g. depression, anxiety and REM sleep behavior disorder. This study was designed to establish the first locus coeruleus α-synucleinopathy mouse model, which should provide sufficient information about the time-course of noradrenergic neurodegeneration, replicate cardinal histopathological features of the human Parkinson's disease neuropathology and finally lead to robust histological markers, which are sufficient to assess the pathological changes in a quantitative and qualitative way...
May 10, 2018: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/29716614/lewy-body-like-alpha-synuclein-inclusions-trigger-reactive-microgliosis-prior-to-nigral-degeneration
#10
Megan F Duffy, Timothy J Collier, Joseph R Patterson, Christopher J Kemp, Kelvin C Luk, Malú G Tansey, Katrina L Paumier, Nicholas M Kanaan, D Luke Fischer, Nicole K Polinski, Olivia L Barth, Jacob W Howe, Nishant N Vaikath, Nour K Majbour, Omar M A El-Agnaf, Caryl E Sortwell
BACKGROUND: Converging evidence suggests a role for microglia-mediated neuroinflammation in Parkinson's disease (PD). Animal models of PD can serve as a platform to investigate the role of neuroinflammation in degeneration in PD. However, due to features of the previously available PD models, interpretations of the role of neuroinflammation as a contributor to or a consequence of neurodegeneration have remained elusive. In the present study, we investigated the temporal relationship of neuroinflammation in a model of synucleinopathy following intrastriatal injection of pre-formed alpha-synuclein fibrils (α-syn PFFS)...
May 1, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29704482/new-hsf1-inducer-as-a-therapeutic-agent-in-a-rodent-model-of-parkinson-s-disease
#11
Irina V Ekimova, Daria V Plaksina, Yuri F Pastukhov, Ksenia V Lapshina, Vladimir F Lazarev, Elena R Mikhaylova, Sergey G Polonik, Bibhusita Pani, Boris A Margulis, Irina V Guzhova, Evgeny Nudler
Molecular chaperone HSP70 (HSPA1A) has therapeutic potential in conformational neurological diseases. Here we evaluate the neuroprotective function of the chaperone in a rat model of Parkinson's disease (PD). We show that the knock-down of HSP70 (HSPA1A) in dopaminergic neurons of the Substantia nigra causes an almost 2-fold increase in neuronal death and multiple motor disturbances in animals. Conversely, pharmacological activation of HSF1 transcription factor and enhanced expression of inducible HSP70 with the echinochrome derivative, U-133, reverses the process of neurodegeneration, as evidenced by а increase in the number of tyrosine hydroxylase-containing neurons, and prevents the motor disturbances that are typical of the clinical stage of the disease...
April 25, 2018: Experimental Neurology
https://www.readbyqxmd.com/read/29679389/down-regulation-of-natural-resistance-associated-macrophage-protein-1-nramp1-is-associated-with-1-methyl-4-phenyl-1-2-3-6-tetrahydropyridine-mptp-1-methyl-4-phenylpyridinium-mpp-induced-%C3%AE-synuclein-accumulation-and-neurotoxicity
#12
K-C Wu, H-H Liou, C-Y Lee, C-J Lin
AIMS: The accumulation of α-synuclein is a hallmark in the pathogenesis of Parkinson's disease (PD). Natural resistance-associated macrophage protein-1 (Nramp1) was previously shown to contribute to the degradation of extracellular α-synuclein in microglia under conditions of iron overload. This study was aimed at investigating the role of Nramp1 in α-synuclein pathology in the neurone under 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)/1-methyl-4-phenylpyridinium (MPP+ ) treatment...
April 21, 2018: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/29673913/epothilone-d-inhibits-microglia-mediated-spread-of-alpha-synuclein-aggregates
#13
Dario Valdinocci, Gary D Grant, Tracey C Dickson, Dean L Pountney
Multiple System Atrophy (MSA) is a progressive neurodegenerative disease characterized by chronic neuroinflammation and widespread α-synuclein (α-syn) cytoplasmic inclusions. Neuroinflammation associated with microglial cells is typically located in brain regions with α-syn deposits. The potential link between microglial cell migration and the transport of pathological α-syn protein in MSA was investigated. Qualitative analysis via immunofluorescence of MSA cases (n = 4) revealed microglial cells bearing α-syn inclusions distal from oligodendrocytes bearing α-syn cytoplasmic inclusions, as well as close interactions between microglia and oligodendrocytes bearing α-syn, suggestive of a potential transfer mechanism between microglia and α-syn bearing cells in MSA and the possibility of microglia acting as a mobile vehicle to spread α-syn between anatomically connected brain regions...
June 2018: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/29656363/2-pentadecyl-2-oxazoline-reduces-neuroinflammatory-environment-in-the-mptp-model-of-parkinson-disease
#14
Marika Cordaro, Rosalba Siracusa, Rosalia Crupi, Daniela Impellizzeri, Alessio Filippo Peritore, Ramona D'Amico, Enrico Gugliandolo, Rosanna Di Paola, Salvatore Cuzzocrea
Current pharmacological management of Parkinson disease (PD) does not provide for disease modification, but addresses only symptomatic features. Here, we explore a new approach to neuroprotection based on the use of 2-pentadecyl-2-oxazoline (PEA-OXA), the oxazoline derivative of the fatty acid amide signaling molecule palmitoylethanolamide (PEA), in an experimental model of PD. Daily oral treatment with PEA-OXA (10 mg/kg) significantly reduced behavioral impairments and neuronal cell degeneration of the dopaminergic tract induced by four intraperitoneal injections of the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on 8-week-old male C57 mice...
April 14, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29624735/cx3cr1-deficiency-exacerbates-alpha-synuclein-a53t-induced-neuroinflammation-and-neurodegeneration-in-a-mouse-model-of-parkinson-s-disease
#15
Sara Castro-Sánchez, Ángel J García-Yagüe, Tresa López-Royo, Maria Casarejos, José Luis Lanciego, Isabel Lastres-Becker
Parkinson's disease (PD) is the second most common neurodegenerative disorder characterized by the degeneration of dopaminergic neurons of the substantia nigra and the accumulation of protein aggregates, called Lewy bodies, where the most abundant is alpha-synuclein (α-SYN). Mutations of the gene that codes for α-SYN (SNCA), such as the A53T mutation, and duplications of the gene generate cases of PD with autosomal dominant inheritance. As a result of the association of inflammation with the neurodegeneration of PD, we analyzed whether overexpression of wild-type α-SYN (α-SYNWT ) or mutated α-SYN (α-SYNA53T ) are involved in the neuronal dopaminergic loss and inflammation process, along with the role of the chemokine fractalkine (CX3CL1) and its receptor (CX3CR1)...
April 6, 2018: Glia
https://www.readbyqxmd.com/read/29568078/taurine-protects-dopaminergic-neurons-in-a-mouse-parkinson-s-disease-model-through-inhibition-of-microglial-m1-polarization
#16
Yuning Che, Liyan Hou, Fuqiang Sun, Cong Zhang, Xiaofang Liu, Fengyuan Piao, Dan Zhang, Huihua Li, Qingshan Wang
Microglia-mediated neuroinflammation is implicated in multiple neurodegenerative disorders, including Parkinson's disease (PD). Hence, the modulatioein of sustained microglial activation may have therapeutic potential. This study is designed to test the neuroprotective efficacy of taurine, a major intracellular free β-amino acid in mammalian tissues, by using paraquat and maneb-induced PD model. Results showed that mice intoxicated with paraquat and maneb displayed progressive dopaminergic neurodegeneration and motor deficits, which was significantly ameliorated by taurine...
March 22, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29560431/cd4-t-cells-react-to-local-increase-of-%C3%AE-synuclein-in-a-pathology-associated-variant-dependent-manner-and-modify-brain-microglia-in-absence-of-brain-pathology
#17
Mads N Olesen, Josefine R Christiansen, Steen Vang Petersen, Poul Henning Jensen, Wojciech Paslawski, Marina Romero-Ramos, Vanesa Sanchez-Guajardo
We have previously shown that immunological processes in the brain during α-synuclein-induced neurodegeneration vary depending on the presence or absence of cell death. This suggests that the immune system is able to react differently to the different stages of α-synuclein pathology. However, it was unclear whether these immune changes were governed by brain processes or by a direct immune response to α-synuclein modifications. We have herein locally increased the peripheral concentration of α-synuclein or its pathology-associated variants, nitrated or fibrillar, to characterize the modulation of the CD4 T cell pool by α-synuclein and brain microglia in the absence of any α-synuclein brain pathology...
January 2018: Heliyon
https://www.readbyqxmd.com/read/29546836/single-chain-fv-antibodies-for-targeting-neurodegenerative-diseases
#18
Kin Yen Chia, Khuen Yen Ng, Rhun Yian Koh, Soi Moi Chye
Protein misfolding and aggregation have been considered the common pathological hallmarks for a number of neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). These abnormal proteins aggregation damage mitochondria and induce oxidative stress and resulting neuronal cell death. Prolong neuronal damage activates microglia and astrocytes, development of inflammation reaction and further promotes neurodegeneration. Thus, elimination of abnormal proteins aggregation without eliciting any adverse effects are the main treatment strategies...
March 15, 2018: CNS & Neurological Disorders Drug Targets
https://www.readbyqxmd.com/read/29497361/silencing-alpha-synuclein-in-mature-nigral-neurons-results-in-rapid-neuroinflammation-and-subsequent-toxicity
#19
Matthew J Benskey, Rhyomi C Sellnow, Ivette M Sandoval, Caryl E Sortwell, Jack W Lipton, Fredric P Manfredsson
Human studies and preclinical models of Parkinson's disease implicate the involvement of both the innate and adaptive immune systems in disease progression. Further, pro-inflammatory markers are highly enriched near neurons containing pathological forms of alpha synuclein (α-syn), and α-syn overexpression recapitulates neuroinflammatory changes in models of Parkinson's disease. These data suggest that α-syn may initiate a pathological inflammatory response, however the mechanism by which α-syn initiates neuroinflammation is poorly understood...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29473513/the-role-of-lrrk2-in-neurodegeneration-of-parkinson-disease
#20
Qin Rui, Haibo Ni, Di Li, Rong Gao, Gang Chen
The leucine-rich repeat kinase 2 (LRRK2) gene and α-synuclein gene (SNCA) are the key influence factors of Parkinson's disease (PD). It is reported that dysfunction of LRRK2 may influence the accumulation of α-synuclein and its pathology to alter cellular functions and signaling pathways by the kinase activation of LRRK2. The accumulation of α-synuclein is one of the main stimulants of microglias acitiviton. Microglias are macrophages resided in the brain, and activation of microglials is believed to contribute to neuroinflammation and neuronal death in PD...
February 22, 2018: Current Neuropharmacology
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