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Times Cited: 17
Times Cited: 17
Times Cited
Times Co-cited
Similarity
Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice.
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Triggering of inflammasome by aggregated α-synuclein, an inflammatory response in synucleinopathies.
Gaia Codolo, Nicoletta Plotegher, Tommaso Pozzobon, Marco Brucale, Isabella Tessari, Luigi Bubacco, Marina de Bernard. PLoS One 2013
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Aggregated alpha-synuclein activates microglia: a process leading to disease progression in Parkinson's disease.
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MPTP-driven NLRP3 inflammasome activation in microglia plays a central role in dopaminergic neurodegeneration.
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Activation of MyD88-dependent TLR1/2 signaling by misfolded α-synuclein, a protein linked to neurodegenerative disorders.
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Reactive microglia are positive for HLA-DR in the substantia nigra of Parkinson's and Alzheimer's disease brains.
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Activation and regulation of the inflammasomes.
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Interleukin-1 beta and interleukin-6 are elevated in the cerebrospinal fluid of Alzheimer's and de novo Parkinson's disease patients.
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The NALP3 inflammasome is involved in the innate immune response to amyloid-beta.
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Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes.
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Synuclein activates microglia in a model of Parkinson's disease.
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Neuron-released oligomeric α-synuclein is an endogenous agonist of TLR2 for paracrine activation of microglia.
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Fyn kinase regulates misfolded α-synuclein uptake and NLRP3 inflammasome activation in microglia.
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Systemic activation of NLRP3 inflammasome and plasma α-synuclein levels are correlated with motor severity and progression in Parkinson's disease.
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Human caspase-4 and caspase-5 regulate the one-step non-canonical inflammasome activation in monocytes.
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Interleukin-1 beta, interleukin-6, epidermal growth factor and transforming growth factor-alpha are elevated in the brain from parkinsonian patients.
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Caspase-4 mediates non-canonical activation of the NLRP3 inflammasome in human myeloid cells.
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Caspase-1 causes truncation and aggregation of the Parkinson's disease-associated protein α-synuclein.
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Unbalanced calcium channel activity underlies selective vulnerability of nigrostriatal dopaminergic terminals in Parkinsonian mice.
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Innate immune activation in neurodegenerative disease.
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Microglial responses to dopamine in a cell culture model of Parkinson's disease.
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NLRP3 inflammasome activation downstream of cytoplasmic LPS recognition by both caspase-4 and caspase-5.
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The IL-1β phenomena in neuroinflammatory diseases.
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Parkinson's disease, dementia with Lewy bodies and multiple system atrophy are alpha-synucleinopathies.
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Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome.
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Pathological α-synuclein exacerbates the progression of Parkinson's disease through microglial activation.
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Inflammasome-induced IL-1β secretion in microglia is characterized by delayed kinetics and is only partially dependent on inflammatory caspases.
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DOPAL derived alpha-synuclein oligomers impair synaptic vesicles physiological function.
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Editor's Highlight: Nlrp3 Is Required for Inflammatory Changes and Nigral Cell Loss Resulting From Chronic Intragastric Rotenone Exposure in Mice.
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Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity.
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NLRP3 inflammasome activation drives tau pathology.
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Microglia in neurodegeneration.
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The microglial NLRP3 inflammasome is activated by amyotrophic lateral sclerosis proteins.
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Neurotoxic reactive astrocytes are induced by activated microglia.
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NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice.
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Meta-analysis of published studies identified eight additional common susceptibility loci for Crohn's disease and ulcerative colitis.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.