Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. Signal., 17 November 2009
Vol. 2, Issue 97, p. ec372
[DOI: 10.1126/scisignal.297ec372]

EDITORS' CHOICE

Neuroscience Sleep and Alzheimer’s Disease

Stella M. Hurtley

Science, AAAS, Cambridge CB2 1LQ, UK

Accumulation of β-amyloid (Aβ) in the brain is thought to be the initiating event in the pathogenesis of Alzheimer’s disease (AD). Aβ is a peptide secreted in a soluble monomeric form predominantly by neurons, and its aggregation into toxic forms is concentration dependent. Synaptic activity regulates the release of Aβ in vivo. However, how physiological and environmental processes are involved in regulation of Aβ levels is not understood. Kang et al., by performing sleep-wake studies in freely behaving animals concomitant with in vivo microdialysis, found that brain interstitial fluid levels of Aβ were significantly correlated with wakefulness and negatively correlated with sleep. Furthermore, relatively short-term (3 weeks) sleep deprivation markedly accelerated amyloid plaque deposition in amyloid precursor protein transgenic mice. Thus, sleep-wake behavior is linked to Aβ levels, and abnormal sleep may be linked to AD pathogenesis.

J.-E. Kang, M. M. Lim, R. J. Bateman, J. J. Lee, L. P. Smyth, J. R. Cirrito, N. Fujiki, S. Nishino, D. M. Holtzman, Amyloid-β dynamics are regulated by orexin and the sleep-wake cycle. Science 326, 1005–1007 (2009). [Abstract] [Full Text]

Citation: S. M. Hurtley, Sleep and Alzheimer’s Disease. Sci. Signal. 2, ec372 (2009).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882