TY  - GEN
T1  - Genetic interactions in a C. elegans sod-1 ALS model: glutamatergic neuron degeneration
AU  - Osborne, Jennifer F
AU  - Yanagi, Katherine S
AU  - Hart, Anne C
DO  - 10.17912/micropub.biology.000338
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000338/
AB  - Amyotrophic lateral sclerosis (ALS) is a fatal degenerative motor neuron disease. While the mechanisms underlying motor neuron death in ALS are not well understood, mutations in over 25 genes can cause this disease (Marangi and Traynor 2015). It remains unclear which, if any, of these genes act in the same disease-associated pathway(s), or if they act in the same pathway(s) as genes associated with the related disorder, frontotemporal dementia (FTD) (Ling et al. 2013). The first ALS-causing gene to be identified was superoxide dismutase 1 (SOD1), a regulator of cytoplasmic redox homeostasis (Rosen et al. 1993). We can begin to construct a pathway for neurodegeneration through SOD1 by identifying genes whose loss of function (LOF) modifies the level of degeneration in a C. elegans SOD1 ALS model. This will contribute to our understanding of whether ALS/FTD genes act in a single or multiple pathways to cause disease.
PY  - 2021
JO  - microPublication Biology
ER  -