TDP-43 secretion in the context of inflammatory stimulation have not yet been studied, but these existing studies indicate that other changes in EV or recipient cell protein composition occurring in TDP-43 proteinopathies, perhaps as a result of changes to proteostasis and autophagy, could significantly modulate the effect of EV-associated TDP-43 on a variety of different cell types in the brain and spinal cord. This evidence concerns the gene TARDBP and proteostasis deficiencies.