Optogenetic Restoration of Disrupted Slow Oscillations Halts Amyloid Deposition and Restores Calcium Homeostasis in an Animal Model of Alzheimer’s Disease

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Optogenetic Restoration of Disrupted Slow Oscillations Halts Amyloid Deposition and Restores Calcium Homeostasis in an Animal Model of Alzheimer’s Disease

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Title: Optogenetic Restoration of Disrupted Slow Oscillations Halts Amyloid Deposition and Restores Calcium Homeostasis in an Animal Model of Alzheimer’s Disease
Author: Kastanenka, Ksenia V.; Hou, Steven S.; Shakerdge, Naomi; Logan, Robert; Feng, Danielle; Wegmann, Susanne; Chopra, Vanita; Hawkes, Jonathan M.; Chen, Xiqun; Bacskai, Brian J.

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Citation: Kastanenka, Ksenia V., Steven S. Hou, Naomi Shakerdge, Robert Logan, Danielle Feng, Susanne Wegmann, Vanita Chopra, Jonathan M. Hawkes, Xiqun Chen, and Brian J. Bacskai. 2017. “Optogenetic Restoration of Disrupted Slow Oscillations Halts Amyloid Deposition and Restores Calcium Homeostasis in an Animal Model of Alzheimer’s Disease.” PLoS ONE 12 (1): e0170275. doi:10.1371/journal.pone.0170275. http://dx.doi.org/10.1371/journal.pone.0170275.
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Abstract: Slow oscillations are important for consolidation of memory during sleep, and Alzheimer’s disease (AD) patients experience memory disturbances. Thus, we examined slow oscillation activity in an animal model of AD. APP mice exhibit aberrant slow oscillation activity. Aberrant inhibitory activity within the cortical circuit was responsible for slow oscillation dysfunction, since topical application of GABA restored slow oscillations in APP mice. In addition, light activation of channelrhodopsin-2 (ChR2) expressed in excitatory cortical neurons restored slow oscillations by synchronizing neuronal activity. Driving slow oscillation activity with ChR2 halted amyloid plaque deposition and prevented calcium overload associated with this pathology. Thus, targeting slow oscillatory activity in AD patients might prevent neurodegenerative phenotypes and slow disease progression.
Published Version: doi:10.1371/journal.pone.0170275
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5257003/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:31731823
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