Evidence map›Paper›PMID 31114516›Full record

ArticleFrontiers in psychiatry2019

Regulation of Tau Protein on the Antidepressant Effects of Ketamine in the Chronic Unpredictable Mild Stress Model.

Gehua Wen, Hui Yao, Yanning Li, Runtao Ding, Xinghua Ren, Yaqing Tan, Weishu Ren, Hao Yu, Xiaoni Zhan, Xiaolong Wang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  11. Deregulated Transcription and Proteostasis in AdultInternational journal of molecular sciences · 2023
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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

15 authors at 3 institutions in 1 country.

Gehua WenSchool of Forensic Medicine, China Medical University, Shenyang, China.
Hui YaoSchool of Forensic Medicine, China Medical University, Shenyang, China.
Yanning LiDepartment of Forensic Medicine, School of Basic Medicine, Gannan Medical University, Ganzhou, China.
Runtao DingSchool of Forensic Medicine, China Medical University, Shenyang, China.
Xinghua RenSchool of Forensic Medicine, China Medical University, Shenyang, China.
Yaqing TanSchool of Forensic Medicine, China Medical University, Shenyang, China.
Weishu RenSchool of Forensic Medicine, China Medical University, Shenyang, China.
Hao YuSchool of Forensic Medicine, China Medical University, Shenyang, China.
Xiaoni ZhanSchool of Forensic Medicine, China Medical University, Shenyang, China.
Xiaolong WangSchool of Forensic Medicine, China Medical University, Shenyang, China.
Enyu XuSchool of Forensic Medicine, China Medical University, Shenyang, China.
Jun YaoSchool of Forensic Medicine, China Medical University, Shenyang, China.
Guohua ZhangSchool of Forensic Medicine, China Medical University, Shenyang, China.
Yan LuKey Laboratory of Health Ministry in Congenital Malformation, the Affiliated Sheng Jing Hospital of China Medical University, Shenyang, China.
Xu WuSchool of Forensic Medicine, China Medical University, Shenyang, China.
China Medical University · CNGannan Medical University · CNSheng Jing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tau protein is known to play an important role in maintaining microtubule assembly and stabilization, and maintaining the normal morphology of neurons, but several studies have found that chronic stress leads to Tau hyperphosphorylation. A large number of clinical trials have found that ketamine, which is an N-methyl-D-aspartate receptor antagonist, produces a rapid, long-lasting, and potent antidepressant effect in patients suffering from major depression. This rapid antidepressant effect of ketamine, which involves many mechanisms, has attracted wide attention. However, the relationship between ketamine's antidepressant effects and Tau protein has rarely been examined. We used C57BL/6 and Tau KO mice exposed to 42 days of chronic unpredictable mild stress (the CUMS model) to investigate the effect of ketamine on behavioral changes and synaptic functioning of the hippocampus. The results showed that a single treatment of ketamine rapidly relieved the CUMS-induced anhedonia, depression-like, and anxious behaviors of the C57BL/6 mice. The abnormal behaviors were accompanied by increased levels of specific alterations of hyperphosphorylated Tau protein in cytoplasm and synapse in the hippocampus of the C57BL/6 mice, but ketamine reduced the aggregation of hyperphosphorylated Tau protein only in the synapse. We also found that CUMS exposure reduced the levels of GluA1 and PSD95 in the hippocampus of the C57BL/6 mice and that these deficits were reversed by ketamine. However, the Tau KO mice did not develop any stress-induced depressive behaviors or deficits of hippocampal function. The antidepressant effect of ketamine may decrease the levels of hyperphosphorylated Tau protein in synapse of C57BL/6 mice.

Indexed as

depressionhippocampusketaminesynapseTau protein phosphorylation

Identifiers

PMID31114516
PMCPMC6503093
OpenAlexW2943332100

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.