Glial activation colocalizes with structural abnormalities in amyotrophic lateral sclerosis

Abstract

Increased uptake of the glial marker [¹¹C]-PBR28 colocalizes with changes in FA and cortical thinning. This suggests a link between disease mechanisms (gliosis and inflammation) and structural changes (cortical thinning and white and gray matter changes). In this multimodal neuroimaging work, we provide an in vivo model to investigate the pathogenesis of ALS.