VPS35 and proteostasis deficiencies: Given that the APA of the retromer components VPS35 and VPS26B is altered upon TDP-43 knockdown [12], and that loss of these proteins is prevalent in neurodegenerative disease [28,29], we set out to explore the ramifications of TDP-43 dysfunction on these retromer components to uncover a potential mechanistic link between TDP-43 loss of function and retromer dysfunction in TDP-43 proteinopathies.