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Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer's disease mice

Citation

Woodhouse, A and Fernandez-Martos, CM and Atkinson, RAK and Hanson, KA and Collins, JM and O'Mara, AR and Terblanche, N and Skinner, MW and Vickers, JC and King, AE, Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer's disease mice, BMC Anesthesiology, 18, (1) Article 47. ISSN 1471-2253 (2018) [Refereed Article]


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Copyright Statement

© The Author(s) 2018. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) http://creativecommons.org/licenses/by/4.0/

DOI: doi:10.1186/s12871-018-0509-5

Abstract

Background: There is increasing interest in whether anesthetic agents affect the risk or progression of Alzheimer's disease (AD). To mitigate many of the methodological issues encountered in human retrospective cohort studies we have used a transgenic model of AD to investigate the effect of propofol on AD pathology.

Methods: Six month-old amyloid precursor protein/presenilin 1 (APP/PS1) transgenic AD mice and control mice were exposed to 3 doses of propofol (200 mg/kg) or vehicle, delivered at monthly intervals.

Results: There was no difference in the extent of β-amyloid (Aβ) immunolabeled plaque deposition in APP/PS1 mice in vehicle versus propofol treatment groups. We also detected no difference in plaque-associated synapse loss in APP/PS1 mice following repeat propofol exposure relative to vehicle. Western blotting indicated that there was no difference in post-synaptic density protein 95, synaptophysin or glutamic acid decarboxylase 65/67 expression in control or APP/PS1 mice subjected to repeat propofol treatment relative to vehicle.

Conclusions: These data suggest that repeat propofol anesthesia may not exacerbate plaque deposition or associated synapse loss in AD. Interestingly, this data also provides some of the first evidence suggesting that repeat propofol exposure in adult wild-type mice does not result in robust long-term alterations in the levels of key excitatory and inhibitory synaptic markers.

Item Details

Item Type:Refereed Article
Keywords:Alzheimer’s disease, glutamic acid decarboxylase, synapse, synaptophysin, beta-amyloid plaques
Research Division:Biomedical and Clinical Sciences
Research Group:Neurosciences
Research Field:Cellular nervous system
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Woodhouse, A (Dr Adele Woodhouse)
UTAS Author:Fernandez-Martos, CM (Dr Carmen Fernandez-Martos)
UTAS Author:Atkinson, RAK (Dr Rachel Atkinson)
UTAS Author:Hanson, KA (Miss Kelsey Hanson)
UTAS Author:Collins, JM (Dr Jessica Collins)
UTAS Author:O'Mara, AR (Mr Aidan O'Mara)
UTAS Author:Terblanche, N (Dr Nico Terblanche)
UTAS Author:Skinner, MW (Dr Marcus Skinner)
UTAS Author:Vickers, JC (Professor James Vickers)
UTAS Author:King, AE (Professor Anna King)
ID Code:126481
Year Published:2018
Web of Science® Times Cited:3
Deposited By:Menzies Institute for Medical Research
Deposited On:2018-06-14
Last Modified:2019-08-05
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