Parkinson's disease and the gut: 'the wheel is come full circle'.

It is both ironic and remarkable that now, almost 200 years later, the question of interaction between the gut and the brain in Parkinson’s disease (PD) has resurfaced to become the subject of a veritable tsunami of fascinating and tremendously important research that has potential ramifications not only for understanding the pathophysiology of PD but also for its treatment and even its diagnosis. During the past 30 years, gastrointestinal (GI) dysfunction has gained recognition as one of the more frequent and troublesome nonmotor features of PD [2, 3] and pathology within the enteric nervous system (ENS), including Lewy body formation and alphasynuclein deposition, has been identified as part of the disorder [4–6]. Loss of dopamine neurons within the ENS also has been reported [6]. Braak et al. have proposed that PD actually has its genesis within the ENS and spreads from there via the vagus nerve to the central nervous system (CNS), initially establishing a beach-