Conclusions
Generally, the genetic study of sleep related disorders still lags behind other medical fields, although in recent years some progress has been made. Only a few GWASs have been performed in sleep disorders, and while basic genetic twin and familial studies had been performed in the past, there are very few studies that applied next generation sequencing technologies on families with sleep-related disorders. So far, there is no evidence for overlap in genetic predisposition for PD and either insomnia, EDS, OSA or circadian sleep-wake cycle disruption. In addition, there is no known overlap between RLS/PLMS genetic markers and PD, although this should be further studied.
In contrast, there is convincing evidence that the genetic basis of PD and RBD overlap, at least partially. Since we now know that the vast majority of cases of RBD have in fact a synucleinopathy in progress, this is not surprising. Of note, although not surprising, these observations linking some PD genetic markers and RBD may have importance for future studies and clinical trials. For instance, when asymptomatic carriers of GBA mutations are being followed up, screening for RBD should be considered for early detection of conversion to a synucleinopathy. Such population of GBA mutation carriers with RBD could be ideal for future clinical trials, since they are highly likely to convert to PD or another synucleinopathy. More genetic studies on RBD are required to identify additional genetic factors that are either shared with PD or unique to RBD, which will allow better characterization of this population.
