Evidence map›Paper›PMID 24725331›Full record

ArticleTranslational neurodegeneration2014

Chronic treatment with anesthetic propofol attenuates β-amyloid protein levels in brain tissues of aged mice.

Yiying Zhang, Haijun Shao, Yuanlin Dong, Celeste A Swain, Buwei Yu, Weiming Xia, Zhongcong Xie

Open access · goldAbstract read
In one paragraph

Article in Translational neurodegeneration, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Experimental laboratory models as tools for understanding modifiable dementia risk.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Yiying Zhang *Geriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 149 13th St., Room 4310, Charlestown, MA 02129-2060, USA.
Haijun Shao *Geriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 149 13th St., Room 4310, Charlestown, MA 02129-2060, USA.
Yuanlin DongGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 149 13th St., Room 4310, Charlestown, MA 02129-2060, USA.
Celeste A SwainGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 149 13th St., Room 4310, Charlestown, MA 02129-2060, USA.
Buwei YuDepartment of Anesthesiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 200025 Shanghai, P.R. China.
Weiming XiaDepartment of Veterans Affairs, Medical Research and Development Service and Geriatric Research, Education and Clinical Center, Bedford, MA 01730, UK.
Zhongcong XieGeriatric Anesthesia Research Unit, Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, 149 13th St., Room 4310, Charlestown, MA 02129-2060, USA.
Massachusetts General Hospital · USGeriatric Research Education and Clinical Center · USHarvard University · USRuijin Hospital · CN

Funding

Pathogenesis of Postoperative Cognitive DysfunctionR01AG041274 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI Zhongcong Xie, Guang Yang · 2012 to 2026
$6.7M
General Anesthesia and Alzheimer's Disease NeuropathogenesisR01GM088801 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI XIE, ZHONGCONG · 2009 to 2017
$3.1M
The Role of Alzheimer's-associated Abeta in POD and POCDR21AG038994 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI XIE, ZHONGCONG · 2011 to 2012
$412k
NIA NIH HHS R01 AG041274NIA NIH HHS R21 AG038994NIGMS NIH HHS R01 GM088801
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common form of dementia. At the present time, however, AD still lacks effective treatments. Our recent studies showed that chronic treatment with anesthetic propofol attenuated brain caspase-3 activation and improved cognitive function in aged mice. Accumulation of β-amyloid protein (Aβ) is a major component of the neuropathogenesis of AD dementia and cognitive impairment. We therefore set out to determine the effects of chronic treatment with propofol on Aβ levels in brain tissues of aged mice. Propofol (50 mg/kg) was administrated to aged (18 month-old) wild-type mice once a week for 8 weeks. The brain tissues of mice were harvested one day after the final propofol treatment. The harvested brain tissues were then subjected to enzyme-linked immunosorbent assay (ELISA) and Western blot analysis. Here we report that the propofol treatment reduced Aβ (Aβ40 and Aβ42) levels in the brain tissues of the aged mice. Moreover, the propofol treatment decreased the levels of β-site amyloid precursor protein cleaving enzyme (the enzyme for Aβ generation), and increased the levels of neprilysin (the enzyme for Aβ degradation) in the brain tissues of the aged mice. These results suggested that the chronic treatment with propofol might reduce brain Aβ levels potentially via decreasing brain levels of β-site amyloid precursor protein cleaving enzyme, thus decreasing Aβ generation; and via increasing brain neprilysin levels, thus increasing Aβ degradation. These preliminary findings from our pilot studies have established a system and postulated a new hypothesis for future research.

Identifiers

PMID24725331
PMCPMC3989795
OpenAlexW2132078712

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.