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- W2007086514 abstract "Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease associated with motor neuron degeneration, muscle weakness, paralysis and finally death. The proposed mechanisms of ALS include glutamate excitotoxicity, oxidative stress, inflammation, mitochondrial dysfunction, apoptosis and proteasomal dysfunction. Although numerous pathological mechanisms have been explained, ALS remains incurable disease because of failure of clinical trials and lack of any effective therapy. The rapid advancement in genetic discoveries in ALS emphasizes the point that ALS is a multi-subtype syndrome rather than a single disease. This can be argued as one of the single reason why many previous therapeutic drug trials have failed. Efforts to develop novel ALS treatments which target specific pathomechanisms are currently being pursued. Herein, we review the recent discovery and preclinical characterization of neuroprotective compounds and compare their effects on disease onset, duration and survival. Furthermore, the structure-activity relationships of these agents are analyzed with the overall goal of developing a screening strategy for future clinical applications." @default.
- W2007086514 created "2016-06-24" @default.
- W2007086514 creator A5065791366 @default.
- W2007086514 date "2009-01-01" @default.
- W2007086514 modified "2023-09-25" @default.
- W2007086514 title "Controlling neuroinflammation through glial cells as viable target for the therapy to slow neurodegeneration in ALS" @default.
- W2007086514 doi "https://doi.org/10.1016/j.neures.2009.09.1662" @default.
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