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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: From mechanisms to future therapy: a synopsis of isolated REM sleep behavior disorder as early synuclein-related disease

Fig. 1

Synucleinopathic degeneration of REM sleep circuits are hypothesized to underlie RBD. Alpha-synuclein aggregation begins in the caudal brainstem and propagates from cell to cell in a caudal-rostral fashion. At prodromal stages of disease, pathology initially develops within the brainstem substrates for REM atonia, including the sublaterodorsal tegmental (SLD) neurons and ventral medulla (vM) neurons. During healthy REM sleep, SLD cells excite vM cells that inhibit spinal motoneurons to induce motor atonia. In RBD, α-syn-mediated dysfunction of these cells leads to loss of REM sleep atonia and the motor behaviors of RBD. Eventually, pathology spreads rostrally towards regions classically associated with the synucleinopathies such as the substantia nigra pars compacta (SNpc) and corticolimbic circuits, where it causes the cardinal motor and cognitive manifestations of these disorders. Figure created with BioRender.com

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Molecular Neurodegeneration

ISSN: 1750-1326