Analyzing non-motor symptoms in Parkinson’s disease (PD) leads to critically re-define and update the disorder itself. The present Editorial encompasses epidemiological and clinical studies on PD patients joined with experimental findings to provide a novel definition of PD based on clinical, neuroanatomical and neurobiological findings. In fact, the plethora of symptoms described in PD patients are due to specific anatomical alterations which cluster in specific disease phenotypes. These PDs differ for disease onset and progression, disease severity and specific cluster of non-motor disturbances. Despite the variety of PD phenotypes, it is now well established that in almost all PD subgroups (except those autosomic recessive selective disorders exemplified by Parkin disease) a core anatomical defnition exists recruiting a variety of brainstem monoamine nuclei. Such a variety of PD pathologies can be defined as monoamine brainstem disorder (MBD).
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