Increased local uptake of TSPO tracers (such as 11C-PK11195 and 11C-PBR28) was consistently detected in the motor cortex, prefrontal cortex, pons, and thalami of sALS patients, colocalizing with structural abnormalities of both grey and white matter and showing significant correlations with clinical measures of UMN burden [322, 323].Similar findings were shown in ALS patients with pathogenic genetic variations in the SOD1 gene, even in the presymptomatic phases [324]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.