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

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.
Authors	Ksenia V Kastanenka, Steven S Hou, Naomi Shakerdge, Robert Logan, Danielle Feng, Susanne Wegmann, Vanita Chopra, Jonathan M Hawkes, Xiqun Chen, Brian J Bacskai
Journal	PloS one (PLoS One) Vol. 12 Issue 1 Pg. e0170275 ( 2017) ISSN: 1932-6203 [Electronic] United States
PMID	28114405 (Publication Type: Journal Article)
Chemical References	Amyloid gamma-Aminobutyric Acid Calcium
Topics	Alzheimer Disease (genetics, metabolism) Amyloid (metabolism) Animals Calcium (metabolism) Disease Models, Animal Down-Regulation Homeostasis Humans Mice Mice, Transgenic Optogenetics gamma-Aminobutyric Acid (metabolism)

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