About this Research Topic
Parkinson's disease (PD) is a neurodegenerative disorder that affects 1.5% of the global population over 65 years of age. The hallmark feature of PD is the degeneration of dopamine neurons in the substantia nigra pars compacta (SNc) and a consequent striatal dopamine deficiency. The pathogenesis of PD remains unclear.
Despite tremendous growth in recent years in our knowledge of the molecular basis of PD and the molecular pathways of cell death important questions remain regarding why are SNc cells especially vulnerable, which mechanisms underlie progressive SNc cell loss or what do Lewy bodies or alpha-synuclein reveal about disease progression. Understanding the different vulnerability of the dopaminergic neurons from midbrain regions and the mechanisms whereby pathology becomes widespread are primary objectives of basic and clinical research in PD.
This current Frontiers Research Topic will discuss the etiopathogenesis of PD, presenting a series of papers that provide up-to-date, state-of-the-art information on molecular and cellular mechanisms involved in the neurodegeneration process in Parkinson Disease, the role of activation of functional anatomical organization of the basal ganglia and in particular habitual vs goal directed systems as a factor of neuronal vulnerability, the possibility that PD is a prion disease and how genetic factors linked to familial and sporadic forms of PD.
We shall welcome experts in the field to contribute original research articles, as well as review articles or case reports that will stimulate the continuing efforts to understand the cell and physiological mechanisms underlying the origin of PD.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.