It is not clear how changes in miR-128 may contribute to the various proteinopathies, and several fundamental questions remain unanswered: Are these changes a consequence of the neuropathological phenotype (e.g., accumulation of Aβ or α-synuclein), or are they involved in the disease pathogenesis, and its dysregulation triggers the neuropathological phenotype? This evidence concerns the gene SNCA and proteostasis deficiencies.