“…These studies revealed sensory-driven compensatory mechanisms in cortico-thalamo-cortical circuits (Bezard et al, 2003;Escola et al, 2003;Pessiglione et al, 2003), but it remains unclear to what extent these animal models can be generalized to human Parkinson's disease. More recently, neuroimaging studies in non-manifesting carriers of mutations known to cause monogenetic forms of Parkinson's disease, such as Parkin (PARK2) or PINK1 (PARK6) mutations (Broussolle et al, 2000;Hilker et al, 2001;Khan et al, 2002aKhan et al, , b, 2005bWalter et al, 2004;Buhmann et al, 2005;Baumer et al, 2007;Binkofski et al, 2007;Hagenah et al, 2007Hagenah et al, , 2008Schweitzer et al, 2007;van Nuenen et al, 2009a, b;Reetz et al, 2010;Saunders-Pullman et al, 2010), have been used to map cerebral changes occurring before the clinical onset of Parkinson's disease (Farrer, 2006). Non-manifesting carriers of these mutations showed structural and functional alterations similar to those observed in idiopathic Parkinson's disease, for example, nigrostriatal and premotor dysfunctions.…”