Neurodegenerative diseases, such as AD characterized by Aβ and tau accumulation, PD associated with α-synuclein aggregates, and ALS marked by superoxide dismutase 1 (SOD 1) misfolding, are increasingly understood in the context of sEVs involvement [45, 113, 129]. This evidence concerns the gene SOD1 and amyotrophic lateral sclerosis.