Evidence map›Paper›PMID 32335546›Full record

ArticleAging2020

Autophagy prevents hippocampal α-synuclein oligomerization and early cognitive dysfunction after anesthesia/surgery in aged rats.

Ning Yang, Zhengqian Li, Dengyang Han, Xinning Mi, Miao Tian, Taotao Liu, Yue Li, Jindan He, Chongshen Kuang, Yiyun Cao and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

14 authors.

Ning YangDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Zhengqian LiDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Dengyang HanDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Xinning MiDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Miao TianChinese Traditional and Herbal Drugs Editorial Office, Tianjin Institute of Pharmaceutical Research, Tianjin 300193, China.
Taotao LiuDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Yue LiDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Jindan HeDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Chongshen KuangDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
Yiyun CaoDepartment of Anesthesiology, Shanghai Sixth People's Hospital East Affiliated with Shanghai University of Medicine and Health Sciences, Shanghai 200233, China.
Lunxu LiDepartment of Anesthesiology, Peking University International Hospital, Beijing 102200, China.
Cheng NiDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.
John Q WangDepartment of Anesthesiology, University of Missouri Kansas City, School of Medicine, Kansas, MO 64110, USA.
Xiangyang GuoDepartment of Anesthesiology, Peking University Third Hospital, Beijing 100191, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stress-induced α-synuclein aggregation, especially the most toxic species (oligomers), may precede synaptic and cognitive dysfunction. Under pathological conditions, α-synuclein is degraded primarily through the autophagic/lysosomal pathway. We assessed the involvement of autophagy in α-synuclein aggregation and cognitive impairment following general anesthesia and surgical stress. Autophagy was found to be suppressed in the aged rat hippocampus after either 4-h propofol anesthesia alone or 2-h propofol anesthesia during a laparotomy surgery. This inhibition of autophagy was accompanied by profound α-synuclein oligomer aggregation and neurotransmitter imbalances in the hippocampus, along with hippocampus-dependent cognitive deficits. These events were not observed 18 weeks after propofol exposure with or without surgical stress. The pharmacological induction of autophagy using rapamycin markedly suppressed α-synuclein oligomerization, restored neurotransmitter equilibrium, and improved cognitive behavior after prolonged anesthesia or anesthesia combined with surgery. Thus, both prolonged propofol anesthesia alone and propofol anesthesia during surgery impaired autophagy, which may have induced abnormal hippocampal α-synuclein aggregation and neurobehavioral deficits in aged rats. These findings suggest that the activation of autophagy and the clearance of pathological α-synuclein oligomers may be novel strategies to ameliorate the common occurrence of postoperative cognitive dysfunction.

Indexed as

alpha-SynucleinAnesthesiaAnimalsAutophagyCognition DisordersDisease Models, AnimalHippocampusMaleNeuronsPostoperative ComplicationsRatsSurgical Procedures, Operativealpha-Synucleinautophagyhippocampusoligomerizationpostoperative cognitive dysfunction (POCD)α-synuclein

Identifiers

PMID32335546
PMCPMC7202547

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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.