HTT and juvenile Huntington disease: Nevertheless, the elucidation of the mechanisms involved in αSyn transcellular transmission will be instrumental not only for the development of novel therapies for PD but also for the understanding of the “prion-like” properties of amyloid-beta (Aβ), tau and Huntingtin, all of them transmissible aggregation-prone proteins with a long history in neurodegenerative diseases such as Alzheimer and Huntington's diseases, respectively (Brettschneider et al., 2015).