Microglia-mediated neurotoxicity: uncovering the molecular mechanisms
By M. Block, L. Zecca, Jau-Shyong Hong. Nature Reviews Neuroscience, 2007
4,009 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/b9609598dee6678369796285e4e9d74033513333
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In Immunology
- B. Barres
- Helmut Kettenmann
- C. Varol
- Steffen Jung
- Melinda E Lull
- M. Goldberg
- M. Tansey
- Chuen-Mao Yang
In Molecular Biology
- Chuen-Mao Yang
- Ruey-Horng Shih
- M. Mouradian
- M. Schwartz
- V. Dias
- Yuanyuan Tang
- Chen-Yu Wang
- G. Martino
In Neurology
- B. Barres
- Helmut Kettenmann
- Melinda E Lull
- S. A. Liddelow
- M. Tansey
- M. Goldberg
- S. Lehnardt
- U. Hanisch
Citations in the corpus
- Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord (2009, background): “, matrix metalloproteinases (MMPs)], and nitric oxide, all of which are able to kill neurons and glia (Block et al., 2007).”
- Reactive Astrocytes: Production, Function, and Therapeutic Potential. (2017, background): “…characterized by upregulation of inflammatory mediators such as Tnf (Tumor Necrosis Factor), Il1b (Interleukin 1 beta), and reactive oxygen species (see Block et al., 2007) to immunosuppressive ‘‘M2-like’’ phenotypes characterized by upregulation of Chil3 (Chitinase-like 3), Fzd1 (Frizzled class…”
- Progress Towards Biocompatible Intracortical Microelectrodes for Neural Interfacing Applications (2014, background): “glycosylphosphatidylinositol-anchored membrane glycoprotein), and other receptor-mediated pathways [119, 120].”
- Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. (2012, neutral): “Chronic microglial activation is considered to be the most damaging response of microglia to injury (Block et al., 2007).”
- Selective Neuronal Vulnerability to Oxidative Stress in the Brain (2010, neutral): “For example, microglia, the principal mediator of infl ammation in the CNS, release a large amount of ROS/RNS upon activation (Colton and Gilbert, 1987; Moss and Bates, 2001; Liu et al., 2002; Block et al., 2007), leading to OS increases and further neuronal damage.”
- Inflammatory Cytokines in Depression: Neurobiological Mechanisms and Therapeutic Implications (2013, background): “…al., 2003), inducible NO synthase (iNOS) (Possel et al., 2000, Lu et al., 2012), reactive oxygen and nitrogen species (ROS/RNS) (Qin et al., 2004, Block et al., 2007), and MCP-1/CCL2 (Kim et al., 2011), a chemokine involved in attracting peripheral immune cells into the brain (see Figure…”
- Normal gut microbiota modulates brain development and behavior (2011, background): “Recent data indicate that pattern recognition receptors expressed on the microglia surface characterize one of the primary, common pathways by which neurotoxin signals affect neuronal tissues (34).”
- Role of Microglia in Neurotrauma (2010, neutral): “to identify and react to noxious stimuli and harmful events.(10) Microglia also express receptors for a number of”
- Microglial Activation & Chronic Neurodegeneration (2010, background): “Reactive microgliosis-chronic response to a single stimulus Although microglial activation was initially perceived as a transient event,(31) it is now believed to be chronic and culpable in the propagation of disease.(1,94,157) Reports have shown that microglia can remain chronically activated(140,1”