Wild-type microglia extend survival in PU.1 knockout mice with familial amyotrophic lateral sclerosis

By D. Beers, J. Henkel, Qin Xiao, Weihua Zhao, Jinghong Wang, A. Yen, L. Siklós, S. Mckercher, S. Appel. Proceedings of the National Academy of Sciences of the United States of America, 2006

750 citations recorded by the source corpus.

Subfields: Neurology

View Paper: https://www.semanticscholar.org/paper/96ef84e3586ff79dd5f31cb680a1b200ea0dee47

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In Neurology

Citations in the corpus

Microglia induce motor neuron death via the classical NF-κB pathway in amyotrophic lateral sclerosis (2014, positive): “Landmark studies have shown selective removal of the causal mutant SOD1 gene from myeloid cells in the slow-progressing SOD1-G37R mice (Boillé e et al., 2006) or repopulating the fastprogressing SOD1-G93A model with WT myeloid cells delays disease progression (Beers et al., 2006).”
Non–cell autonomous toxicity in neurodegenerative disorders: ALS and beyond (2009, background): “Similarly, bone marrow transplantation to generate complete replacement of mutant SOD1-expressing microglial cells with nontransgenic ones did not affect disease onset, but slowed progression (Beers et al., 2006).”
Origin and differentiation of microglia (2013, methodology): “Briefly, this mouse model expresses a tamoxifenactivated MER-Cre-MER recombinase gene under the control of one of the endogenous promoters of the runt-related transcription factor 1 (Runx1) locus (Samokhvalov et al., 2007).”
Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases (2015, background): “sion in microglia could slow disease progression and prolong the survival of mSOD1 or mSOD1 mice [133, 134].”
Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. (2010, background): “Although expression of mutant SOD1 restricted to either astrocytes [183] or microglia [77]”
Microglia activation triggers astrocyte-mediated modulation of excitatory neurotransmission (2011, positive): “To functionally show the involvement of microglia in the regulation of EPSCs, we assessed the effect of LPS application in brain slices from mice deficient in the myeloid-specific transcription factor Pu-1 that lack microglia (27) (Fig.”
The blood-brain barrier in health and chronic neurodegenerative disorders. (2008, positive): “Neurovascular Unit The current model of ALS disease suggests that toxicity derived from microglia and astrocytes contributes to disease progression and motor neuron degeneration (Boillée et al., 2006a, 2006b; Beers et al., 2006; Di Giorgio et al., 2007; Nagai et al., 2007).”