Indeed, a series of recent, exciting studies have shown that the pathologic hallmarks of various PMDs, including Alzheimer's, Parkinson's, Huntington's diseases, and some forms of systemic amyloidosis, can be induced under experimental conditions by administration of tissue homogenates carrying the respective misfolded proteins (Xing et al., 2001; Lundmark et al., 2002; Meyer - Luehmann et al., 2006; Clavaguera et al., 2009; Ren et al., 2009; Eisele et al., 2010; Grad et al., 2011;
Luk et al., 2012; Morales et al., 2012; Mougenot et al., 2012; Stöhr et al., 2012; Iba et al., 2013).
Experimental studies and a growing body of evidence has emerged demonstrating that synthetic α synuclein fibrils (both human and murine) are capable of «seeding» and propagating α synuclein pathology not only in α synuclein transgenic mouse models but importantly in non-transgenic (WT) neuronal cultures and mice (
Luk, K.C.
et al., 2012a;
Luk, K.C.
et al., 2012b; Volpicelli - Daley, L.A.
et al., 2014).