Transthyretin (ATTR) amyloidosis is a multisystem disease caused by misfolding and aggregation of the plasma protein transthyretin (TTR) into insoluble amyloid fibrils in various organs [1]. This condition results either from age-related proteostatic failure in wild-type ATTR (ATTRwt) amyloidosis or from destabilizing mutations in variant ATTR (ATTRv) amyloidosis [1]. Amyloid deposition disrupts tissue structure and function, leading clinically to predominant cardiomyopathy in ATTRwt (ATTR-CM) and to polyneuropathy with or without cardiomyopathy in ATTRv disease (ATTR-PN and ATTR-mixed) (Fig.
