This is different to typical pathology in TDP-43 proteinopathies where nuclear TDP-43 is depleted leading to loss of nuclear TDP-43 function, and TDP-43 is translocated to the cytoplasm leading to gain-of-function effects [2, 11, 75, 76] Hence, the low abundance of cytoplasmic translocation of TDP-43 is a limitation with the present study and it is possible that other results would have been detected if more AgRP neurons would have displayed cytoplasmic translocation of TDP-43. The gene discussed is AGRP; the disease is proteostasis deficiencies.