Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer’s disease mice
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...
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| Format: | Article |
| Language: | English |
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BMC
2018-04-01
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| Series: | BMC Anesthesiology |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s12871-018-0509-5 |
| _version_ | 1819297919348506624 |
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| author | 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 |
| author_facet | 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 |
| author_sort | Adele Woodhouse |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-24T05:21:39Z |
| format | Article |
| id | doaj.art-9d31865b280e468a93007bf83d1b1f0f |
| institution | Directory Open Access Journal |
| issn | 1471-2253 |
| language | English |
| last_indexed | 2024-12-24T05:21:39Z |
| publishDate | 2018-04-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Anesthesiology |
| spelling | doaj.art-9d31865b280e468a93007bf83d1b1f0f2022-12-21T17:13:27ZengBMCBMC Anesthesiology1471-22532018-04-011811810.1186/s12871-018-0509-5Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer’s disease miceAdele Woodhouse0Carmen Maria Fernandez-Martos1Rachel Alice Kathryn Atkinson2Kelsey Anne Hanson3Jessica Marie Collins4Aidan Ryan O’Mara5Nico Terblanche6Marcus Welby Skinner7James Clement Vickers8Anna Elizabeth King9Wicking Dementia Research and Education Centre , University of TasmaniaWicking Dementia Research and Education Centre , University of TasmaniaWicking Dementia Research and Education Centre , University of TasmaniaWicking Dementia Research and Education Centre , University of TasmaniaWicking Dementia Research and Education Centre , University of TasmaniaWicking Dementia Research and Education Centre , University of TasmaniaTasmanian Health Service, Royal Hobart HospitalDepartment of Health and Human Services Tasmania, Royal Hobart HospitalWicking Dementia Research and Education Centre , University of TasmaniaWicking Dementia Research and Education Centre , University of TasmaniaAbstract 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.http://link.springer.com/article/10.1186/s12871-018-0509-5Alzheimer’s diseaseβ-amyloid plaquesSynapseSynaptophysinGlutamic acid decarboxylase |
| spellingShingle | 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 Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer’s disease mice BMC Anesthesiology Alzheimer’s disease β-amyloid plaques Synapse Synaptophysin Glutamic acid decarboxylase |
| title | Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer’s disease mice |
| title_full | Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer’s disease mice |
| title_fullStr | Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer’s disease mice |
| title_full_unstemmed | Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer’s disease mice |
| title_short | Repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in APP/PS1 Alzheimer’s disease mice |
| title_sort | repeat propofol anesthesia does not exacerbate plaque deposition or synapse loss in app ps1 alzheimer s disease mice |
| topic | Alzheimer’s disease β-amyloid plaques Synapse Synaptophysin Glutamic acid decarboxylase |
| url | http://link.springer.com/article/10.1186/s12871-018-0509-5 |
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