**4. Conclusions and future directions**

Astrocytes clearly contribute to ALS decrease progression in both neuroinflammation and excitotoxicity. An intriguing aspect of astrocytes in ALS disease pathology is whether the mutant SOD1 astrocytic properties, of LIGHT dependent cell death and diminished GluR2 editing for example, are also important in other ALS causing mutations and in sporadic cases of ALS. Initial work performed implies that these characteristics are not solely dependent on mutant SOD1 in patients. In addition, both mechanisms in which astrocytes function seem successfully targetable in mice. Future research may benefit from further assessing the role of also non-SOD1 ALS causing mutations in astrocytes on ALS and optimizing therapeutic strategies against neuroinflammation and excitotoxicity.
