Systemic amyloidoses represent a group of rare diseases that are often underdiagnosed due to their multifaceted symptomatic picture. In these multisystem diseases, misfolded fibrillar proteins are deposited extracellularly in various organs, resulting in a successive loss of their function and integrity. To date, 42 different proteins have been identified as amyloidogenic; at least 19 of them can cause systemic disease. Two of these proteins have been within the focus of this work. Transthyretin amyloidosis (ATTR amyloidosis) is characterized by progressive deposition of the plasma protein transthyretin (TTR) in the myocardium, peripheral nerves and other tissues, which ultimately leads to congestive heart failure, polyneuropathy and death. There are two forms of ATTR amyloidosis, wild-type ATTR (ATTRwt) and hereditary ATTR (ATTRv) amyloidosis.
