Transmissible human proteopathies: an expanding field

Prions are considered the prototype of transmissible proteopathies, and this property has for many decades been considered unique. More recently the transmissibility of other misfolded proteins, notably Aβ, tau and synuclein, has been recognized. Initially, the transmission of these proteins was shown experimentally but the relevance for humans was debated. The co-transmission of Aβ with prions through medical procedures involving preparations derived from cadaveric human tissues, such as human growth hormone treatment, dura mater transplants or the use of neurosurgical instruments carrying traces of Aβ protein has fundamentally changed the opinion in the field. In this article, we will summarize the key features of the most common neurodegenerative diseases involving protein misfolding and their established or potential role in disease transmission