Sleep the Toxins Away

Deep sleep is nowadays recognized as a potential regulator of brain waste removal. Boosting sleep has proven to clear protein deposits that hallmark Alzheimer’s disease. Daniela Noain and Christian Baumann from the Neurology Department at the University Hospital Zurich wondered if deep sleep could also alleviate the accumulation of alpha-synuclein, a protein that is associated with the pathology of Parkinson’s disease.

The researchers administered a deep sleep-inducing drug for four months in animal models of Parkinson’s disease with synuclein pathology. In one of the models, they additionally tested whether sleep deprivation would, on the contrary, worsen the brain pathology. To understand the mechanisms behind the pathology, Noain and her colleagues explored a myriad of molecular pathways potentially mediating sleep-triggered neuroprotection. They found that the brains from Parkinson’s mice that underwent deep sleep enhancement were less burdened with toxic alpha-synuclein deposits. In fact, the pathology lowered to the level of healthy individuals. Sleep deprivation, on the other side, worsened the brain pathology dramatically. The brain waste removal process along other neuroprotective mechanisms appeared to be boosted after deep sleep enhancement. 

The ultimate goal of this preclinical research is to find therapeutic alternatives to counteract the onset and progression of neurodegenerative diseases characterized by protein deposition, such as Parkinson’s disease. Although studies in human subjects will have to explore the feasibility and efficacy of the approach in clinical populations, these encouraging results open new disease-modifying research avenues for Parkinson’s patients.

By: Daniela Noain, Neurology Department, University Hospital Zurich, University of Zurich.

Reference: Morawska, M.M., Moreira, C.G., Ginde, V.R., Valko, P.O., Weiss, T., Büchele, F., Imbach, L.L., Masneuf, S., Kollarik, S., Prymaczok, N., Gerez, J.A., Riek, R., Baumann, C.R., Noain, D. Slow-wave sleep affects synucleinopathy and regulates proteostatic processes in mouse models of Parkinson’s disease. Sci Transl Med (2021).

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