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Parkinson disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy are synucleinopathies, characterized by neuronal loss, gliosis and the abnormal deposition of α-synuclein in vulnerable areas of the nervous system. Neurodegeneration begins however several years before clinical onset of motor, cognitive or autonomic symptoms. The isolated form of REM sleep behavior disorder (RBD), a parasomnia with dream enactment behaviors and excessive muscle activity during REM sleep, is an early stage synucleinopathy. The neurophysiological hallmark of RBD is REM sleep without atonia (RWSA), i.e. the loss of physiological muscle atonia during REM sleep. RBD pathophysiology is not fully clarified yet, but clinical and basic science suggest that ɑ-syn pathology begins in the lower brainstem where REM atonia circuits are located, including the sublaterodorsal tegmental/subcoeruleus nucleus and the ventral medulla, then propagates rostrally to brain regions such as the substantia nigra, limbic system, cortex. Genetically, there is only a partial overlap between RBD, PD and DLB, and individuals with iRBD may represent a specific subpopulation. A genome-wide association study identified five loci, which all seem to revolve around the GBA1 pathway. iRBD patients often show subtle motor, cognitive, autonomic and/or sensory signs, neuroimaging alterations as well as biofluid and tissue markers of neurodegeneration (in particular pathologic α-synuclein aggregates), which can be useful for risk stratification. Patients with iRBD represent thus the ideal population for neuroprotective/neuromodulating trials. This review provides insights into these aspects, highlighting and substantiating the central role of iRBD in treatment development strategies for synucleinopathies. [ABSTRACT FROM AUTHOR]

Walking ability is essential for human survival and health. Its basic rhythm is mainly generated by the central pattern generator of the spinal cord. The rhythmic stimulation of music to the auditory center affects the cerebral cortex and other higher nerve centers, and acts on the central pattern generator. By means of rhythm entrainment, the central pattern generator can produce walking rhythm synchronized with music rhythm, control muscle tension, and then regulate human gait. Basal ganglia dysfunction is the main cause of abnormal gait in patients with Parkinson's disease. Music therapy provides external rhythmic stimulation, recruits neural networks to bypass the basal ganglia and synchronizes gait with external rhythms in both time and space through auditory-motor neural networks, helping to promote the improvement of abnormal gait patterns in patients with Parkinson's disease. [ABSTRACT FROM AUTHOR]