Microglia acquire distinct activation profiles depending on the degree of alpha-synuclein neuropathology in a rAAV based model of Parkinson's disease.
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Glia and alpha-synuclein in neurodegeneration: A complex interactionThe complex relationships between microglia, alpha-synuclein, and LRRK2 in Parkinson's diseaseTen years and counting: moving leucine-rich repeat kinase 2 inhibitors to the clinicVaccination strategies for Parkinson disease: induction of a swift attack or raising tolerance?M1 and M2 immune activation in Parkinson's Disease: Foe and ally?Neuroimmunological processes in Parkinson's disease and their relation to α-synuclein: microglia as the referee between neuronal processes and peripheral immunityIsothiocyanates Are Promising Compounds against Oxidative Stress, Neuroinflammation and Cell Death that May Benefit Neurodegeneration in Parkinson's DiseaseMorphological and behavioral impact of AAV2/5-mediated overexpression of human wildtype alpha-synuclein in the rat nigrostriatal systemExposure of neonatal rats to alcohol has differential effects on neuroinflammation and neuronal survival in the cerebellum and hippocampus.Glial innate immunity generated by non-aggregated alpha-synuclein in mouse: differences between wild-type and Parkinson's disease-linked mutants.Molecular Targets for PET Imaging of Activated Microglia: The Current Situation and Future Expectations.Abrogation of α-synuclein-mediated dopaminergic neurodegeneration in LRRK2-deficient rats.Progressive neurodegeneration or endogenous compensation in an animal model of Parkinson's disease produced by decreasing doses of alpha-synuclein.Fcγ receptors are required for NF-κB signaling, microglial activation and dopaminergic neurodegeneration in an AAV-synuclein mouse model of Parkinson's disease.Microglial activation correlates with disease progression and upper motor neuron clinical symptoms in amyotrophic lateral sclerosisExpression of human A53T alpha-synuclein in the rat substantia nigra using a novel AAV1/2 vector produces a rapidly evolving pathology with protein aggregation, dystrophic neurite architecture and nigrostriatal degeneration with potential to model trAAV2/7 vector-mediated overexpression of alpha-synuclein in mouse substantia nigra induces protein aggregation and progressive dose-dependent neurodegeneration.Apoptosis signal-regulating kinase 1 modulates the phenotype of α-synuclein transgenic mice.Expression of mutant alpha-synuclein modulates microglial phenotype in vitroNeonatal exposure to lipopolysaccharide enhances vulnerability of nigrostriatal dopaminergic neurons to rotenone neurotoxicity in later life.Role of α-synuclein in inducing innate and adaptive immunity in Parkinson disease.Inflammatory effects of highly pathogenic H5N1 influenza virus infection in the CNS of mice.Changes in the miRNA-mRNA Regulatory Network Precede Motor Symptoms in a Mouse Model of Multiple System Atrophy: Clinical ImplicationsActivin A Inhibits MPTP and LPS-Induced Increases in Inflammatory Cell Populations and Loss of Dopamine Neurons in the Mouse Midbrain In Vivo.Upregulation of mesencephalic astrocyte-derived neurotrophic factor in glial cells is associated with ischemia-induced glial activation.Epigallocatechin-3-gallate: a useful, effective and safe clinical approach for targeted prevention and individualised treatment of neurological diseases?Human neuromelanin: an endogenous microglial activator for dopaminergic neuron deathNeonatal exposure to lipopolysaccharide enhances accumulation of α-synuclein aggregation and dopamine transporter protein expression in the substantia nigra in responses to rotenone challenge in later lifeInfiltrating T lymphocytes reduce myeloid phagocytosis activity in synucleinopathy model.Neonatal systemic exposure to lipopolysaccharide enhances susceptibility of nigrostriatal dopaminergic neurons to rotenone neurotoxicity in later life.Distinct Pattern of Microgliosis in the Olfactory Bulb of Neurodegenerative Proteinopathies.Activated immune cells in Parkinson's disease.Glial dysfunction in the pathogenesis of α-synucleinopathies: emerging concepts.Imaging of microglia in patients with neurodegenerative disorders.The role of regulatory T cells in neurodegenerative diseases.The role of glia in α-synucleinopathies.Dysfunction of two lysosome degradation pathways of α-synuclein in Parkinson's disease: potential therapeutic targets?The role of inflammation in sporadic and familial Parkinson's disease.T-cell-mediated regulation of neuroinflammation involved in neurodegenerative diseases.Regulation of the Neurodegenerative Process Associated to Parkinson's Disease by CD4+ T-cells.
P2860
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P2860
Microglia acquire distinct activation profiles depending on the degree of alpha-synuclein neuropathology in a rAAV based model of Parkinson's disease.
description
2010 nî lūn-bûn
@nan
2010 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Microglia acquire distinct act ...... model of Parkinson's disease.
@ast
Microglia acquire distinct act ...... model of Parkinson's disease.
@en
Microglia acquire distinct act ...... model of Parkinson's disease.
@nl
type
label
Microglia acquire distinct act ...... model of Parkinson's disease.
@ast
Microglia acquire distinct act ...... model of Parkinson's disease.
@en
Microglia acquire distinct act ...... model of Parkinson's disease.
@nl
prefLabel
Microglia acquire distinct act ...... model of Parkinson's disease.
@ast
Microglia acquire distinct act ...... model of Parkinson's disease.
@en
Microglia acquire distinct act ...... model of Parkinson's disease.
@nl
P2860
P921
P1433
P1476
Microglia acquire distinct act ...... d model of Parkinson's disease
@en
P2093
Deniz Kirik
Fabia Febbraro
P2860
P356
10.1371/JOURNAL.PONE.0008784
P407
P577
2010-01-20T00:00:00Z