LAUSR

Epidemiological studies have demonstrated that sleep disorders are associated with a decline in cognitive performance, productivity, mood, and quality of life, as well as with major social, medical, and economic impacts. At present, the pathophysiology of sleep–wake disturbances in PD remains largely unknown, although the etiology is most likely multifactorial. Alterations of pathophysiological mechanisms are thought to underlie several processes, including sleep–wake regulatory centers, overnight emergence of motor symptoms, adverse effects of antiparkinsonian medications, psychiatric symptoms, and sleep fragmentation caused by multiple factors.[1,2] However, recent genetic studies of PD had identified multiple genes and loci which might be associated with sleep disorders. Genetic studies of rapid eye movement sleep behavior disorder (RBD) offered some new insights that glucocerebrosidase mutations and microtubule‐associated protein tau loci were associated with RBD. Moreover, some genes and genetic loci were associated with restless legs syndrome (RLS) as follows: MEIS1, BTBD9, PTPRD, MAP2K5/SKOR1, TOX3, and RLS1‐8.[3]