This is again in sharp contrast to Thy1-haSN mice that showed early-onset impairments of motor performance . Furthermore we observed increased mortality in Thy1-maSN mice compared to control wildtype littermates . We performed different behavioral studies to determine motor function. Thy1-maSN mice showed no difference in the open field paradigm. Neither velocity nor total activity was changed. Furthermore, no difference could be detected in forelimb grip strength . Motor coordination was assessed using the accelerated rotarod task starting at two months of age. During the first four weeks, Thy1-maSN mice showed impaired motor learning but by 12 weeks of age and after a number of training sessions, the performance of Thy1-maSN mice was indistinguishable from wt mice up to the age of six months . From 6�C7 months onwards, a steady and rapid decline in rotarod performance in Thy1-maSN mice became obvious . Interestingly no difference in light/dark cycle activity, assessed by an actimeter for 48 h, could be detected between Thy1-maSN and wt mice . In order to determine the anxiety of Thy1-maSN mice we performed dark-light box and elevated plus maze experiments . We observed similar latencies and total time spend in the lit compartment between wt and mutants in the dark-light box , suggesting no impact on anxiety. This was fortified using the elevated plus maze . It is remarkable that Thy1-maSN mice displayed a late-onset and much less pronounced motor impairment than transgenic mice expressing the haSN transgene with early-onset and steady decline in motor control . Similar to earlier observations in mice expressing haSN forms we found maSN expressed in many neurons in telencephalon, hippocampus, brainstem, cerebellar Fulvestrant nuclei and spinal cord . The maSN expression in the hippocampus showed an increase in perikaryal and neuritic immunostaining for aSN and cerebellar nuclei respectively . In a substantial neuronal subset expression of the transgene was sufficient for perikaryal and neuritic maSN accumulation, which did not change over time . This is further demonstrated by maSN immunostaining of hippocampal neurons in mice expressing the Thy1-maSN transgene on a mouse genetic background with a disrupted endogenous aSN gene .