GBA1 and proteostasis deficiencies: Even though more genetic and neuropathological studies are needed to establish the relationship of the gut microbiota changes with α-synuclein, leucine-rich repeat kinase 2, or glucocerebrosidase gene expression, as well as with other proteinopathies (i.e., amyloid-beta, tau and TAR DNA binding protein 43), our results suggest that gut dysbiosis may play a role in the different natural history and prognosis of disease related to TD and non-TD phenotypes.