Neuroinflammatory mechanisms in amyotrophic lateral sclerosis pathogenesis

2018 ◽  
Vol 31 (5) ◽  
pp. 635-639 ◽  
Author(s):  
Jason R. Thonhoff ◽  
Ericka P. Simpson ◽  
Stanley H. Appel
2001 ◽  
Vol 21 (02) ◽  
pp. 131-140 ◽  
Author(s):  
Robert H. Brown, Jr ◽  
Wim Robberecht

Brain ◽  
2020 ◽  
Vol 143 (6) ◽  
pp. 1651-1673 ◽  
Author(s):  
Wenting Guo ◽  
Tijs Vandoorne ◽  
Jolien Steyaert ◽  
Kim A Staats ◽  
Ludo Van Den Bosch

Abstract Amyotrophic lateral sclerosis is the most common degenerative disorder of motor neurons in adults. As there is no cure, thousands of individuals who are alive at present will succumb to the disease. In recent years, numerous causative genes and risk factors for amyotrophic lateral sclerosis have been identified. Several of the recently identified genes encode kinases. In addition, the hypothesis that (de)phosphorylation processes drive the disease process resulting in selective motor neuron degeneration in different disease variants has been postulated. We re-evaluate the evidence for this hypothesis based on recent findings and discuss the multiple roles of kinases in amyotrophic lateral sclerosis pathogenesis. We propose that kinases could represent promising therapeutic targets. Mainly due to the comprehensive regulation of kinases, however, a better understanding of the disturbances in the kinome network in amyotrophic lateral sclerosis is needed to properly target specific kinases in the clinic.


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