Unraveling the mechanisms involved in motor neuron degeneration in ALS.

By L. Bruijn, T. Miller, D. Cleveland. Annual Review of Neuroscience, 2004

1,409 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/8bf8963cfd5706533728e3b4c4f636a49b5e3537

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Citations in the corpus

Astrocyte dysfunction in neurological disorders: a molecular perspective (2006, background): “In addition to protein damage as a result of oxidative stress, mutant SOD1 might cause toxicity by the aberrant activation of biochemical pathways, accumulation of protein aggregates and stimulation of caspases in motor neurons and astrocytes (for a review, see Ref”
Astrocytes, from brain glue to communication elements: the revolution continues (2005, neutral): “fcgi?db=gene&cmd=Retrieve&dopt=Graphics&list_uids=20655">SOD1”
NODDI: Practical in vivo neurite orientation dispersion and density imaging of the human brain (2012, background): “, 2000), amyotrophic lateral sclerosis (Bruijn et al., 2004), and Alzheimer's disease (PaulaBarbosa et al.”
Non–cell autonomous effect of glia on motor neurons in an embryonic stem cell–based ALS model (2007, background): “Studies with these animals have led to the identification of intrinsic pathogenic characteristics of ALS motor neurons, including the formation of protein aggregates, cytoskeletal abnormalities, proteosome dysfunction and increased sensitivity to cell death signal”
TDP-43 Proteinopathy and Motor Neuron Disease in Chronic Traumatic Encephalopathy (2010, background): “Whereas 90% to 95% of ALS cases are sporadic, gene mutations in copper/zinc superoxide dismutase 1, senataxin, dynactin, angiogenic, and TAR-DBP (the gene for transactive response DNA-binding protein of 43 kd [TDP-43] on chromosome 1) account for some familial forms of the disease (1, 2).”
Oxidative stress in ALS: key role in motor neuron injury and therapeutic target. (2010, background): “Deletion of either neuronal or inducible nitric oxide synthase has been reported to have no effect on disease progression of mutant SOD1 mice [65] [66] [67], casting doubt on the role of zinc deficiency in mutant SOD1 pathogenesis.”
Current hypotheses for the underlying biology of amyotrophic lateral sclerosis (2009, background): “Because the sporadic and familial forms of ALS are clinically similar, progress in elucidating the mechanisms underlying familial ALS may provide insight into both forms of the disease.(2) Moreover, a recent study identified an aberrant SOD1-containing protein in spinal cord tissue from patients wit”