Aggregated α‐synuclein activates microglia: a process leading to disease progression in Parkinson's disease

By Wei Zhang, Tongguang Wang, Zhongshi Pei, David S. Miller, Xuefei Wu, M. Block, B. Wilson, Wanqin Zhang, Yong-Chun Zhou, Jau-Shyong Hong and 1 more. The FASEB Journal, 2005

1,140 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/6b07b108e99926873c9564300371ca020dd747dc

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In Cellular and Molecular Neuroscience

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Citations in the corpus

Pathological roles of MAPK signaling pathways in human diseases. (2010, background): “production induced by the toxins results in the activation of microglial cells, which subsequently attack neighboring dopaminergic neurons [64–66].”
Exosomal cell-to-cell transmission of alpha synuclein oligomers (2012, background): “Exosome-associated αsyn oligomers are more prone to internalization than exosome-free αsyn oligomers It has been reported that recombinant αsyn or αsyn oligomers can be internalized by cells and result in various cellular effects [18-20,33,67].”
Microglia and inflammation-mediated neurodegeneration: multiple triggers with a common mechanism. (2005, background): “Recently, we have identified a subset of toxins that are selectively toxic to DA neurons through the phagocytic activation of microglia: DEP (Block et al., 2004), LPS (Pei et al., unpublished results), a-synuclein (Zhang et al., 2005), and gp91 (Block et al., unpublished results).”
Alternatively activated microglia and macrophages in the central nervous system. (2015, background): “…disease (Mosher and Wyss-Coray, 2014; Rogers et al., 2007; Solito and Sastre, 2012), Parkinson’s disease (Doorn et al., 2012; Rogers et al., 2007; Zhang et al., 2005) and stroke (Patel et al., 2013), being the MHC-II receptors detected in samples from patients with these disorders as well as…”
Cell-Produced α-Synuclein Is Secreted in a Calcium-Dependent Manner by Exosomes and Impacts Neuronal Survival (2010, background): “It has been reported that recombinant -synuclein can activate microglia cells (Zhang et al., 2005; Su et al., 2008).”
Inflammation as a causative factor in the aetiology of Parkinson's disease (2007, background): “Recently, it has been shown that a-synuclein activates microglia, and in microglia-depleted cultures, low concentrations of a-synuclein fail to induce DA toxicity (Zhang et al., 2005).”
Role of Oxidative Stress in Parkinson's Disease (2013, background): “The addition of aggregated human α-synuclein to a primary mesencephalic neuron-glia culture causes activation of microglia and DAergic neurodegeneration, and this cytotoxicity does not occur in the absence of microglia [44].”
Alpha-synuclein: Pathology, mitochondrial dysfunction and neuroinflammation in Parkinson's disease. (2018, background): “Zhang et al. (2005) first reported that microglial ROS productionwas directly augmented byα-synucleinwithin primary mesencephalic neuron-glia culture systems (Zhang et al., 2005).”
Neuroinflammation in Parkinson’s disease and its potential as therapeutic target (2015, background): “As the disease progresses, molecules such as α-synuclein, ATP and metalloproteinase-3 (MMP-3) released from the degenerating DA neurons will further enhance microglia activation, amplify the neuroinflammatory responses in the brain, and result in the deterioration of the neurodegenerative processes ”