Evidence map›Paper›PMID 42045038›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026

[Modified

Chenchen Xu, Yongsheng Han, Nan Cheng, Jianjian Dong

Abstract readEnglish Abstract
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Chenchen XuInstitute of Neurology, Affiliated Hospital of Institute of Neurology, Center for Xin-An Medicine and Modernization of Traditional Chinese Medicine of IHM, Anhui University of Chinese Medicine, Hefei 230000 China.
Yongsheng HanInstitute of Neurology, Affiliated Hospital of Institute of Neurology, Center for Xin-An Medicine and Modernization of Traditional Chinese Medicine of IHM, Anhui University of Chinese Medicine, Hefei 230000 China.
Nan ChengInstitute of Neurology, Affiliated Hospital of Institute of Neurology, Center for Xin-An Medicine and Modernization of Traditional Chinese Medicine of IHM, Anhui University of Chinese Medicine, Hefei 230000 China.
Jianjian DongInstitute of Neurology, Affiliated Hospital of Institute of Neurology, Center for Xin-An Medicine and Modernization of Traditional Chinese Medicine of IHM, Anhui University of Chinese Medicine, Hefei 230000 China.

Funding

National Natural Science Foundation of China 81904086, 81603596 and 81673948
6 · The paper itself

Abstract

objectivesTo assess the effect of the Modified

methodsThirty-six TX mice were randomized into TX group, TX+MGDD group, C16 group, and C16+MGDD group. In C16 and C16+MGDD group, the mice received daily intraperitoneal injections of 300 μg/kg C16 (a PKR inhibitor) for 30 days, and saline injections were given in the other two groups; after WD modeling, the mice in TX+MGDD and C16+MGDD groups received MGDD gavage for 4 weeks, while the other two groups were given saline gavage. After the treatments, the mice were examined using behavioral tests, followed by immunofluorescence staining, TUNEL staining, TEM, RT-qPCR and Western blotting analysis of the brain tissue.

resultsIn behavioral tests, the mice in C16+MGDD group showed significantly shorter time spent in the perimeter than those in C16 group without significant differences in other parameters. Immunofluorescence staining revealed obviously lowered hippocampal oxidative stress level in C16, TX+MGDD, and C16+MGDD groups compared with TX group. Both MGDD and C16 treatment alone increased the number of hippocampal synapses and vesicles and improved ultrastructural synaptic damages, but their combination exhibited no synergistic effect. The C16+MGDD group showed significantly higher expressions of PSD93, PSD95, synapsin1 and synaptophysin than C16 group, but had comparable PSD93 expression with TX+MGDD group. While the mRNA expressions in the PKR/eIF2α pathway were similar between C16+MGDD and C16 groups, the protein levels of P-eIF2α and CHOP were significantly lower and P-CREB protein level was higher in C16+MGDD group.

conclusionsMGDD improves cognitive dysfunction in WD TX mice possibly by inhibiting the PKR/eIF2α pathway, promoting expressions of synaptic proteins, and improving synaptic structure and function.

Indexed as

CognitionDrugs, Chinese HerbaleIF-2 KinaseEukaryotic Initiation Factor-2Hepatolenticular DegenerationAnimalsDisease Models, AnimalHippocampusMaleMiceSignal TransductionDrugs, Chinese HerbaleIF-2 KinaseEukaryotic Initiation Factor-2protein kinase R, mousecognitive dysfunctionPKR/eIF2α pathwaysynaptic plasticityTongFuYangSuiWilson's disease

Identifiers

PMID42045038
PMCPMC13120979

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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.