Researchers of the Hospital Clínic de Barcelona-Idibaps have shown that isolated rapid eye movement REM sleep behavior disorder (iRBD) is a early stage of neurodegenerative diseases related to the alpha-synuclein protein.
Parkinson’s, dementia with Lewy bodies and multiple system atrophy are some of the synucleinopathies that could originate or be detected in early stages through iRBD, as explained by the Clínic in a statement.
The team has obtained evidence from the study of post-mortem brain tissue, being the first study with more cases where this relationship is confirmed “in a detailed and definitive manner”, which has been published in ‘The Lancet Neurology’.
iRBD is a sleep disorder characterized by nightmares and abnormal behavior during sleep, such as screaming or punching, associated with REM sleep without muscle relaxation. This disorder has previously been considered a precursor to neurodegenerative diseases by this same group of researchers in a line of research that dates back to 2006. However, until now, there was a lack of definitive evidence that could confirm its link with major disorders such as Parkinson’s wave dementia with Lewy bodies.
Early identification of iRBD could serve as biomarker for the progression in alpha-synucleopathies, which is “important in early detection and clinical intervention,” reports Ep.
Furthermore, the identification of multiple coexisting pathologies opens “new opportunities” to design therapies targeting not only alpha-synuclein, but also other pathological proteins.
The study suggests that clinical trials that treat different pathological proteins in combination could be an “promising” strategy to prevent or delay the onset of Parkinson’s and dementia in people with iRBD. “These findings are consistent with previous studies that have suggested that iRBD could be an early manifestation of synucleinopathies, but this study provides the strongest neuropathological evidence to date,” he explains. Gerard Mayà. Furthermore, the researchers found that α-synuclein deposits were not only present in neurons, but also in glial cells (astrocytes and oligodendrocytes), suggesting that glia also play a key role in disease progression.
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