Optogenetic Restoration of Disrupted Slow Oscillations Halts Amyloid Deposition and Restores Calcium Homeostasis in an Animal Model of Alzheimer's Disease
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...
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| Veröffentlicht in: | PloS one 2017-01, Vol.12 (1), p.e0170275-e0170275 |
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| creator | Kastanenka, Ksenia V Hou, Steven S Shakerdge, Naomi Logan, Robert Feng, Danielle Wegmann, Susanne Chopra, Vanita Hawkes, Jonathan M Chen, Xiqun Bacskai, Brian J |
| description | 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. |
| doi_str_mv | 10.1371/journal.pone.0170275 |
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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. 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This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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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.</description><subject>Aberration</subject><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer's disease</subject><subject>Alzheimers disease</subject><subject>Amyloid</subject><subject>Amyloid - metabolism</subject><subject>Amyloid beta-protein</subject><subject>Animal cognition</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Brain</subject><subject>Calcium</subject><subject>Calcium - metabolism</subject><subject>Calcium homeostasis</subject><subject>Calcium ions</subject><subject>Calcium signalling</subject><subject>Cognitive ability</subject><subject>Consolidation</subject><subject>Deposition</subject><subject>Development and progression</subject><subject>Disease Models, 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| subjects | Aberration Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer's disease Alzheimers disease Amyloid Amyloid - metabolism Amyloid beta-protein Animal cognition Animal models Animals Biology and Life Sciences Brain Calcium Calcium - metabolism Calcium homeostasis Calcium ions Calcium signalling Cognitive ability Consolidation Deposition Development and progression Disease Models, Animal Down-Regulation Fourier transforms gamma-Aminobutyric Acid - metabolism Genetic aspects Homeostasis Hospitals Humans Medical research Medical schools Medicine and Health Sciences Memory Mice Mice, Transgenic Neurodegenerative diseases Neurology Optogenetics Oscillations Patients Physiological aspects Proteins Research and Analysis Methods Restoration Rodents Sleep Synchronism Topical application γ-Aminobutyric acid |
| title | 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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