LAUSR

More than 200 years after its initial description by James Parkinson (1817), the disease that now bears his name is still a topic of intense research. Despite remarkable progress in the management of its motor symptoms by pharmacologic dopamine replacement or deep brain stimulation, there is still no cure and all attempts to develop treatments that halt or slow down the relentless progression of the disease have so far failed. Ironically, it is the progress in management of motor symptoms that have made us painfully aware of the huge impact of non-motor symptoms— autonomic disturbances, pain, depression and particularly cognitive decline— have on quality of life in the course of the disease. Given the changing age structure of our society, the number of patients with Parkinson’s disease will inevitably increase greatly over the coming decades (Dorsey and Bloem 2018). A better understanding of the complex pathogenetic networks that contribute to disease risk, progression and the development of late complications is therefore urgently needed in order to develop novel effective treatment strategies that go beyond mere amelioration of the consequences of disturbed motor circuits. Section 1: molecules and cells