Extracellular TTR aggregation and deposition triggers inflammation and oxidative damage5, disruption of calcium homeostasis6, extracellular matrix remodeling7, activation of heat shock response and endoplasmic reticulum (ER) stress pathways6, 8, including common molecular actors and scenarios, that resemble in many features those associated to local amyloidoses affecting the central nervous system such as Alzheimer’s and Parkinson’s diseases. This evidence concerns the gene TTR and amyloidosis.