Blunting neuroinflammation with resolvin D1 prevents early pathology in a rat model of Parkinson’s disease
Neuroinflammation is one of the hallmarks of Parkinson’s disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins....
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| Vydáno v: | Nature communications Ročník 10; číslo 1; s. 3945 - 19 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
Nature Publishing Group UK
02.09.2019
Nature Publishing Group Nature Portfolio |
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| ISSN: | 2041-1723, 2041-1723 |
| On-line přístup: | Získat plný text |
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| Abstract | Neuroinflammation is one of the hallmarks of Parkinson’s disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins. However, the effects of stimulating the resolution of inflammation in PD – to modulate disease progression – still remain unexplored. Here we show that rats overexpressing human α-synuclein (Syn) display altered DA neuron properties, reduced striatal DA outflow and motor deficits prior to nigral degeneration. These early alterations are coupled with microglia activation and perturbations of inflammatory and pro-resolving mediators, namely IFN-γ and resolvin D1 (RvD1). Chronic and early RvD1 administration in Syn rats prevents central and peripheral inflammation, as well as neuronal dysfunction and motor deficits. We also show that endogenous RvD1 is decreased in human patients with early-PD. Our results suggest there is an imbalance between neuroinflammatory and pro-resolving processes in PD.
Resolvins are endogenous lipids with pro-resolving activity. Here the authors find that rats overexpressing human α-synuclein show defects in dopamine signalling before dopamine cell loss, and that this is associated with low Resolvin D1 levels and neuroinflammation. |
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| AbstractList | Neuroinflammation is one of the hallmarks of Parkinson's disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins. However, the effects of stimulating the resolution of inflammation in PD - to modulate disease progression - still remain unexplored. Here we show that rats overexpressing human α-synuclein (Syn) display altered DA neuron properties, reduced striatal DA outflow and motor deficits prior to nigral degeneration. These early alterations are coupled with microglia activation and perturbations of inflammatory and pro-resolving mediators, namely IFN-γ and resolvin D1 (RvD1). Chronic and early RvD1 administration in Syn rats prevents central and peripheral inflammation, as well as neuronal dysfunction and motor deficits. We also show that endogenous RvD1 is decreased in human patients with early-PD. Our results suggest there is an imbalance between neuroinflammatory and pro-resolving processes in PD. Neuroinflammation is one of the hallmarks of Parkinson’s disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins. However, the effects of stimulating the resolution of inflammation in PD – to modulate disease progression – still remain unexplored. Here we show that rats overexpressing human α-synuclein (Syn) display altered DA neuron properties, reduced striatal DA outflow and motor deficits prior to nigral degeneration. These early alterations are coupled with microglia activation and perturbations of inflammatory and pro-resolving mediators, namely IFN-γ and resolvin D1 (RvD1). Chronic and early RvD1 administration in Syn rats prevents central and peripheral inflammation, as well as neuronal dysfunction and motor deficits. We also show that endogenous RvD1 is decreased in human patients with early-PD. Our results suggest there is an imbalance between neuroinflammatory and pro-resolving processes in PD. Resolvins are endogenous lipids with pro-resolving activity. Here the authors find that rats overexpressing human α-synuclein show defects in dopamine signalling before dopamine cell loss, and that this is associated with low Resolvin D1 levels and neuroinflammation. Resolvins are endogenous lipids with pro-resolving activity. Here the authors find that rats overexpressing human α-synuclein show defects in dopamine signalling before dopamine cell loss, and that this is associated with low Resolvin D1 levels and neuroinflammation. Neuroinflammation is one of the hallmarks of Parkinson’s disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins. However, the effects of stimulating the resolution of inflammation in PD – to modulate disease progression – still remain unexplored. Here we show that rats overexpressing human α-synuclein (Syn) display altered DA neuron properties, reduced striatal DA outflow and motor deficits prior to nigral degeneration. These early alterations are coupled with microglia activation and perturbations of inflammatory and pro-resolving mediators, namely IFN-γ and resolvin D1 (RvD1). Chronic and early RvD1 administration in Syn rats prevents central and peripheral inflammation, as well as neuronal dysfunction and motor deficits. We also show that endogenous RvD1 is decreased in human patients with early-PD. Our results suggest there is an imbalance between neuroinflammatory and pro-resolving processes in PD. Resolvins are endogenous lipids with pro-resolving activity. Here the authors find that rats overexpressing human α-synuclein show defects in dopamine signalling before dopamine cell loss, and that this is associated with low Resolvin D1 levels and neuroinflammation. Neuroinflammation is one of the hallmarks of Parkinson’s disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins. However, the effects of stimulating the resolution of inflammation in PD – to modulate disease progression – still remain unexplored. Here we show that rats overexpressing human α-synuclein (Syn) display altered DA neuron properties, reduced striatal DA outflow and motor deficits prior to nigral degeneration. These early alterations are coupled with microglia activation and perturbations of inflammatory and pro-resolving mediators, namely IFN-γ and resolvin D1 (RvD1). Chronic and early RvD1 administration in Syn rats prevents central and peripheral inflammation, as well as neuronal dysfunction and motor deficits. We also show that endogenous RvD1 is decreased in human patients with early-PD. Our results suggest there is an imbalance between neuroinflammatory and pro-resolving processes in PD. Neuroinflammation is one of the hallmarks of Parkinson's disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins. However, the effects of stimulating the resolution of inflammation in PD - to modulate disease progression - still remain unexplored. Here we show that rats overexpressing human α-synuclein (Syn) display altered DA neuron properties, reduced striatal DA outflow and motor deficits prior to nigral degeneration. These early alterations are coupled with microglia activation and perturbations of inflammatory and pro-resolving mediators, namely IFN-γ and resolvin D1 (RvD1). Chronic and early RvD1 administration in Syn rats prevents central and peripheral inflammation, as well as neuronal dysfunction and motor deficits. We also show that endogenous RvD1 is decreased in human patients with early-PD. Our results suggest there is an imbalance between neuroinflammatory and pro-resolving processes in PD.Neuroinflammation is one of the hallmarks of Parkinson's disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link chronic inflammation with failure to resolve early inflammation, a process operated by specialized pro-resolving mediators, including resolvins. However, the effects of stimulating the resolution of inflammation in PD - to modulate disease progression - still remain unexplored. Here we show that rats overexpressing human α-synuclein (Syn) display altered DA neuron properties, reduced striatal DA outflow and motor deficits prior to nigral degeneration. These early alterations are coupled with microglia activation and perturbations of inflammatory and pro-resolving mediators, namely IFN-γ and resolvin D1 (RvD1). Chronic and early RvD1 administration in Syn rats prevents central and peripheral inflammation, as well as neuronal dysfunction and motor deficits. We also show that endogenous RvD1 is decreased in human patients with early-PD. Our results suggest there is an imbalance between neuroinflammatory and pro-resolving processes in PD. |
| ArticleNumber | 3945 |
| Author | Calabresi, Paolo Federici, Mauro Di Lazzaro, Giulia Natale, Giuseppina Picconi, Barbara Calabrese, Valeria Viscomi, Maria Teresa Riess, Olaf D’Amelio, Marcello Nobili, Annalisa Schirinzi, Tommaso Mercuri, Nicola Biagio Ghiglieri, Veronica Chiurchiù, Valerio Bernardini, Sergio Vedele, Francescangelo Marino, Gioia Krashia, Paraskevi Sancesario, Giulia Cordella, Alberto La Barbera, Livia Leuti, Alessandro Campanelli, Federica Pisani, Antonio Serhan, Charles Nicholas Casadei, Nicolas |
| Author_xml | – sequence: 1 givenname: Paraskevi orcidid: 0000-0002-8476-9233 surname: Krashia fullname: Krashia, Paraskevi organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Medicine and Department of Science and Technology for Humans and Environment, University Campus Bio-medico – sequence: 2 givenname: Alberto surname: Cordella fullname: Cordella, Alberto organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Systems Medicine, University of Rome ‘Tor Vergata’ – sequence: 3 givenname: Annalisa surname: Nobili fullname: Nobili, Annalisa organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Medicine and Department of Science and Technology for Humans and Environment, University Campus Bio-medico – sequence: 4 givenname: Livia surname: La Barbera fullname: La Barbera, Livia organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Systems Medicine, University of Rome ‘Tor Vergata’ – sequence: 5 givenname: Mauro orcidid: 0000-0003-4563-1677 surname: Federici fullname: Federici, Mauro organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation – sequence: 6 givenname: Alessandro surname: Leuti fullname: Leuti, Alessandro organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Medicine and Department of Science and Technology for Humans and Environment, University Campus Bio-medico – sequence: 7 givenname: Federica surname: Campanelli fullname: Campanelli, Federica organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation – sequence: 8 givenname: Giuseppina surname: Natale fullname: Natale, Giuseppina organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation – sequence: 9 givenname: Gioia surname: Marino fullname: Marino, Gioia organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation – sequence: 10 givenname: Valeria orcidid: 0000-0002-1127-1741 surname: Calabrese fullname: Calabrese, Valeria organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation – sequence: 11 givenname: Francescangelo surname: Vedele fullname: Vedele, Francescangelo organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Systems Medicine, University of Rome ‘Tor Vergata’ – sequence: 12 givenname: Veronica surname: Ghiglieri fullname: Ghiglieri, Veronica organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Philosophy, Human, Social and Educational Sciences, University of Perugia – sequence: 13 givenname: Barbara surname: Picconi fullname: Picconi, Barbara organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation – sequence: 14 givenname: Giulia surname: Di Lazzaro fullname: Di Lazzaro, Giulia organization: Department of Systems Medicine, University of Rome ‘Tor Vergata’ – sequence: 15 givenname: Tommaso surname: Schirinzi fullname: Schirinzi, Tommaso organization: Department of Systems Medicine, University of Rome ‘Tor Vergata’ – sequence: 16 givenname: Giulia surname: Sancesario fullname: Sancesario, Giulia organization: Department of Clinical and Behavioural Neurology, IRCCS Santa Lucia Foundation – sequence: 17 givenname: Nicolas surname: Casadei fullname: Casadei, Nicolas organization: Institute of Medical Genetics and Applied Genomics, University of Tübingen – sequence: 18 givenname: Olaf surname: Riess fullname: Riess, Olaf organization: Institute of Medical Genetics and Applied Genomics, University of Tübingen – sequence: 19 givenname: Sergio surname: Bernardini fullname: Bernardini, Sergio organization: Department of Experimental Medicine and Surgery, University of Rome ‘Tor Vergata’ – sequence: 20 givenname: Antonio orcidid: 0000-0002-8432-594X surname: Pisani fullname: Pisani, Antonio organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Systems Medicine, University of Rome ‘Tor Vergata’ – sequence: 21 givenname: Paolo surname: Calabresi fullname: Calabresi, Paolo organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Neurology Clinic, Department of Medicine, University of Perugia, Santa Maria della Misericordia Hospital – sequence: 22 givenname: Maria Teresa surname: Viscomi fullname: Viscomi, Maria Teresa organization: Institute of Histology and Embryology, Università Cattolica del Sacro Cuore – sequence: 23 givenname: Charles Nicholas orcidid: 0000-0003-4627-8545 surname: Serhan fullname: Serhan, Charles Nicholas organization: Center for Experimental Therapeutics and Reperfusion Injury, Department of Anaesthesiology, Perioperative and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School – sequence: 24 givenname: Valerio surname: Chiurchiù fullname: Chiurchiù, Valerio organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Medicine and Department of Science and Technology for Humans and Environment, University Campus Bio-medico – sequence: 25 givenname: Marcello surname: D’Amelio fullname: D’Amelio, Marcello organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Medicine and Department of Science and Technology for Humans and Environment, University Campus Bio-medico – sequence: 26 givenname: Nicola Biagio orcidid: 0000-0001-6700-7491 surname: Mercuri fullname: Mercuri, Nicola Biagio email: mercurin@med.uniroma2.it organization: Department of Experimental Neurosciences, IRCCS Santa Lucia Foundation, Department of Systems Medicine, University of Rome ‘Tor Vergata’ |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31477726$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | The Author(s) 2019 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| Snippet | Neuroinflammation is one of the hallmarks of Parkinson’s disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link... Neuroinflammation is one of the hallmarks of Parkinson's disease (PD) and may contribute to midbrain dopamine (DA) neuron degeneration. Recent studies link... Resolvins are endogenous lipids with pro-resolving activity. Here the authors find that rats overexpressing human α-synuclein show defects in dopamine... |
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| Title | Blunting neuroinflammation with resolvin D1 prevents early pathology in a rat model of Parkinson’s disease |
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