Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS)
By D. Howland, Jian Liu, Yijin She, Beth Goad, N. Maragakis, Benjamin Kim, J. Erickson, J. Kulik, Lisa DeVito, G. Psaltis and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2002
846 citations recorded by the source corpus.
Subfields: Genetics, Neurology
View Paper: https://www.semanticscholar.org/paper/3dd8f94ba98bb18ec94fe22de3d991238b289c4b
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In Genetics
In Neurology
- Robert H. Brown
- P. Pasinelli
- Andrea Volterra
- J. Lladó
- S. Przedborski
- Jeffrey D. Rothstein
- D. Bergles
- G. Olmos
Citations in the corpus
- Tumor Necrosis Factor Alpha: A Link between Neuroinflammation and Excitotoxicity (2014, positive): “As an example, in ALS, where neuroinflammation and excitotoxicity are fundamental mechanisms involved in motoneuron degeneration [65, 95], decreased GLT-1 expression has been reported both in patients [96] and rat models [97, 98].”
- Chronic Glutamate Toxicity in Neurodegenerative Diseases—What is the Evidence? (2015, background): “The downregulation of EAAT2 in human ALS is recapitulated in several animal models of ALS including transgenic mice expressing human SOD1 containing the G93A mutation that causes hereditary ALS (Bendotti et al., 2001) or transgenic rats expressing the same mutation (Howland et al., 2002).”
- Molecular biology of amyotrophic lateral sclerosis: insights from genetics (2006, background): “In most cases (∼65%) of SALS, and in transgenic rodent ALS models, there is a profound reduction in the expression and activity of EAAT2 in the cortex and spinal cor”
- Current hypotheses for the underlying biology of amyotrophic lateral sclerosis (2009, background): “In the mid-1990s, defects in astroglia-specific glutamate transporters were identified in a large percentage of sporadic ALS patients,(43) and later in all SOD1 rodent models.(10,44) Astrocytic inclusions are early indicators of SOD1 mutant toxicity, preceding symptom onset and increasing with disea”
- Astrocytes, from brain glue to communication elements: the revolution continues (2005, background): “They show focal loss of the glutamate transporter EAAT2 (Ref”
- β-Lactam antibiotics offer neuroprotection by increasing glutamate transporter expression (2005, background): “GLT1 expression decreases around the onset of clinical diseas”