At the same time, recent studies using a transgenic mouse model expressing SOD1 G93A mutant continue to support an ALS-associated impairment of mitochondrial clearance, which can be due to the overexpression of the translocator protein (TSPO, 18 kDa), an outer mitochondrial membrane protein that is widely used as a marker of neuroinflammation [166]. Here, SOD1 is linked to amyotrophic lateral sclerosis.