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01.12.2018 | Research article | Ausgabe 1/2018 Open Access

BMC Anesthesiology 1/2018

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

Zeitschrift:
BMC Anesthesiology > Ausgabe 1/2018
Autoren:
Adele Woodhouse, Carmen Maria Fernandez-Martos, Rachel Alice Kathryn Atkinson, Kelsey Anne Hanson, Jessica Marie Collins, Aidan Ryan O’Mara, Nico Terblanche, Marcus Welby Skinner, James Clement Vickers, Anna Elizabeth King
Wichtige Hinweise

Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1186/​s12871-018-0509-5) contains supplementary material, which is available to authorized users.

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.
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