The aim of the present study was to (a) investigate the LC and NBM integrity in patients with identical clinical phenotypes underpinned by distinct mechanisms (TDP-43 proteinopathy in presumed-LATE and amyloid/tau pathology in amnestic AD) by combining in vivo MRI assessment of LC-I and NBM volume, (b) explore in a supplementary analysis patients with another type of TDP-43 or tau pathology (FTD) and (c) analyze the relation between LC-I/NBM volume and cognition as well as medial temporal and cortical atrophy in these groups of patients. The gene discussed is TARDBP; the disease is amyloidosis.