Abstract
Recent advances in the genetics of ALS have bolstered hope that a molecular logic for the pathogenesis of the disease is fast approaching. An emerging challenge is the dissection of the common and unique molecular pathways altered by ALS gene mutations. Disease modeling in rodents has yielded many important insights, but as the genetic complexity of the disease grows, additional models with improved speed, cost and genetic tractability will be increasingly necessary. Models such as fruitfly, nematode, and zebrafish have been important for diagramming the molecular pathways that underlie many fundamental biological processes, but have been comparatively underutilized in the study of neurodegeneration. Here we highlight the benefits and opportunities for increased diversity in the models used to study ALS.
Highlights
Even though Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by motor neuron dysfunction, current developments and discoveries lead the way to a better tomorrow for both patients and clinicians
Recently a new drug Redicava received FDA approval [1], and there are more than 3 compounds in Phase III clinical trials, the highest number in ALS research history
Many in the field suggested that complex biology cannot be understood by using simple organisms and using S. cerevisiae or C. elegans for a disease such as ALS, would not reflect effective use of time
Summary
Moving toward a molecular logic for ALSEven though Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by motor neuron dysfunction, current developments and discoveries lead the way to a better tomorrow for both patients and clinicians. The major limitation today is not the absence of data, but understanding the matrix of information generated from many different sources and models [4]. To further understand the impact of genetic mutations on motor neuron survival and degeneration, numerous disease models have been generated.
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