Microglial phenotypes and toll-like receptor 2 in the substantia nigra and hippocampus of incidental Lewy body disease cases and Parkinson's disease patients. - Wikidata - wikimedia - TriplyDB

Microglial phenotypes and toll-like receptor 2 in the substantia nigra and hippocampus of incidental Lewy body disease cases and Parkinson's disease patients.

Microglial phenotypes and toll-like receptor 2 in the substantia nigra and hippocampus of incidental Lewy body disease cases and Parkinson's disease patients.

http://www.wikidata.org/entity/Q34470963

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Molecular Mechanism of Adult Neurogenesis and its Association with Human Brain Diseases Degeneration of Dopaminergic Neurons Due to Metabolic Alterations and Parkinson's Disease Immune phenotypes of microglia in human neurodegenerative disease: challenges to detecting microglial polarization in human brains Oxidative stress and Parkinson's disease Glia and alpha-synuclein in neurodegeneration: A complex interaction Age-dependent neuroinflammation and cognitive decline in a novel Ala152Thr-Tau transgenic mouse model of PSP and AD.The Indispensable Roles of Microglia and Astrocytes during Brain Development Astrocyte-derived tissue Transglutaminase affects fibronectin deposition, but not aggregation, during cuprizone-induced demyelination Translocator Protein-18 kDa (TSPO) Positron Emission Tomography (PET) Imaging and Its Clinical Impact in Neurodegenerative Diseases Hippocampal proliferation is increased in presymptomatic Parkinson's disease and due to microglia.Proliferation in the Alzheimer hippocampus is due to microglia, not astroglia, and occurs at sites of amyloid deposition.Exploring Braak's Hypothesis of Parkinson's Disease.Activation of MyD88-dependent TLR1/2 signaling by misfolded α-synuclein, a protein linked to neurodegenerative disorders.Altered Expression Patterns of Inflammation-Associated and Trophic Molecules in Substantia Nigra and Striatum Brain Samples from Parkinson's Disease, Incidental Lewy Body Disease and Normal Control Cases.Non-cell-autonomous Neurotoxicity of α-synuclein Through Microglial Toll-like Receptor 2 Toll-like receptor 2 is increased in neurons in Parkinson's disease brain and may contribute to alpha-synuclein pathology.Propagation of pathological α-synuclein in marmoset brain.Reduced CA2-CA3 Hippocampal Subfield Volume Is Related to Depression and Normalized by l-DOPA in Newly Diagnosed Parkinson's Disease.Distinct Pattern of Microgliosis in the Olfactory Bulb of Neurodegenerative Proteinopathies.Roles of microglia in brain development, tissue maintenance and repair.Mitochondrial control of cell bioenergetics in Parkinson's disease.Parkinson's disease: Microglial/macrophage-induced immunoexcitotoxicity as a central mechanism of neurodegeneration The Role of Microglia in Retinal Neurodegeneration: Alzheimer's Disease, Parkinson, and Glaucoma.Brain region-specific gene expression profiles in freshly isolated rat microglia.Let's make microglia great again in neurodegenerative disorders.Microglia Gone Rogue: Impacts on Psychiatric Disorders across the Lifespan.Differential α-synuclein expression contributes to selective vulnerability of hippocampal neuron subpopulations to fibril-induced toxicity.Boosting phagocytosis and anti-inflammatory phenotype in microglia mediates neuroprotection by PPARγ agonist MDG548 in Parkinson's disease.Toll-Like Receptor 2 Signaling and Current Approaches for Therapeutic Modulation in Synucleinopathies.Microglial Phagocytosis and Its Regulation: A Therapeutic Target in Parkinson's Disease?Indomethacin promotes survival of new neurons in the adult murine hippocampus accompanied by anti-inflammatory effects following MPTP-induced dopamine depletion.Role of Microglia TLRs in Neurodegeneration Suppression of Presymptomatic Oxidative Stress and Inflammation in Neurodegeneration by Grape-Derived Polyphenols Immunotherapy targeting toll-like receptor 2 alleviates neurodegeneration in models of synucleinopathy by modulating α-synuclein transmission and neuroinflammation Microglia Response During Parkinson's Disease: Alpha-Synuclein Intervention

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P2860

Microglial phenotypes and toll-like receptor 2 in the substantia nigra and hippocampus of incidental Lewy body disease cases and Parkinson's disease patients.

http://www.wikidata.org/entity/Q34470963

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2014 nî lūn-bûn

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2014 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2014 թվականի օգոստոսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Acta neuropathologica communications

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Microglial phenotypes and toll ...... Parkinson's disease patients.

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Anne-Marie van Dam

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Karlijn J Doorn

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Paul J Lucassen

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Tim Moors

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Wilma Dj van de Berg

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P2860

Molecular cloning of CD68, a human macrophage marker related to lysosomal glycoproteins

Staging of brain pathology related to sporadic Parkinson's disease

Microglia: active sensor and versatile effector cells in the normal and pathologic brain

Parkinson's disease: mechanisms and models

The chemokine system in diverse forms of macrophage activation and polarization

Stages in the development of Parkinson's disease-related pathology

Reactive microglia are positive for HLA-DR in the substantia nigra of Parkinson's and Alzheimer's disease brains

Microglia: a sensor for pathological events in the CNS

α-Syn suppression reverses synaptic and memory defects in a mouse model of dementia with Lewy bodies.

Loss of olfaction in de novo and treated Parkinson's disease: possible implications for early diagnosis.

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Benjamin Drukarch

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