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Neurodegenerative disease

A good night's sleep

Nature Reviews Neuroscience volume 8, page 656 (2007)Cite this article

Previously, Morton's laboratory revealed that the R6/2 mouse, which has motor and cognitive deficits that are typical of the human disease, suffers from disrupted sleep–wake patterns, including an increase in daytime activity (wild type mice usually sleep during the day) and a decrease in nocturnal activity. Eventually the sleep–wake cycle disintegrates. Reasoning that disrupted sleep might underlie some of the cognitive deficits, they investigated whether normalizing sleep patterns would improve cognition.

R6/2 mice were previously shown to exhibit altered expression of genes that are associated with circadian pacemaking, including period 2 and prokineticin 2, in their suprachiasmatic nuclei (SCN). However, the authors found that the R6/2 SCN, when it was isolated from the rest of the brain, showed normal firing behaviour and rhythmic fluctuations in gene expression. This implied that regions up or downstream of the SCN are the source of the disrupted sleep patterns.

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ORIGINAL RESEARCH PAPER

  1. Pallier, P. N. et al. Pharmacological imposition of sleep slows cognitive decline and reverses dysregulation of circadian gene expression in a transgenic mouse model of Huntington's disease. J. Neurosci. 27, 7869–7878 (2007)

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  1. Katherine Whalley
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Whalley, K. A good night's sleep. Nat Rev Neurosci 8, 656 (2007). https://doi.org/10.1038/nrn2220

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