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

Woodhouse, A ORCID: 0000-0002-4246-7624, Fernandez-Martos, CM ORCID: 0000-0002-6387-4456, Atkinson, RAK ORCID: 0000-0002-9846-7738, Hanson, KA ORCID: 0000-0002-4230-1827, Collins, JM, O'Mara, AR, Terblanche, NCS ORCID: 0000-0003-3228-0636, Skinner, MW, Vickers, JC ORCID: 0000-0001-5671-4879 and King, AE ORCID: 0000-0003-1792-0965 2018 , 'Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer's disease mice' , BMC Anesthesiology, vol. 18, no. 1 , pp. 1-8 , doi: https://doi.org/10.1186/s12871-018-0509-5.

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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 Type: Article
Authors/Creators:Woodhouse, A and Fernandez-Martos, CM and Atkinson, RAK and Hanson, KA and Collins, JM and O'Mara, AR and Terblanche, NCS and Skinner, MW and Vickers, JC and King, AE
Keywords: Alzheimer’s disease, glutamic acid decarboxylase, synapse, synaptophysin, β-amyloid plaques
Journal or Publication Title: BMC Anesthesiology
Publisher: BioMed Central Ltd.
ISSN: 1471-2253
DOI / ID Number: https://doi.org/10.1186/s12871-018-0509-5
Copyright Information:

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

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