These findings can be explained by several factors: the affinity of amyloid tracers for β-sheet-structured protein such as myelin basic protein, the greater degree of demyelination observed in the DWM in pathological studies, and similar results from previous amyloid PET studies in MS, which demonstrated lower tracer uptake in the DWM areas compared to NAWM in both MS patients and healthy controls [9,11,24]. This evidence concerns the gene MBP and myeloid sarcoma.