Evidence map›Paper›PMID 26974541›Full record

ArticlePloS one2016

Oridonin Attenuates Synaptic Loss and Cognitive Deficits in an Aβ1-42-Induced Mouse Model of Alzheimer's Disease.

Sulei Wang, Linjie Yu, Hui Yang, Chaosheng Li, Zhen Hui, Yun Xu, Xiaolei Zhu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 71 citations in OpenAlex.

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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 2 institutions in 1 country.

Sulei WangDepartment of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, PR China.
Linjie YuDepartment of Neurology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, PR China.
Hui YangDepartment of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, PR China.
Chaosheng LiDepartment of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, PR China.
Zhen HuiDepartment of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, PR China.
Yun XuDepartment of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, PR China.
Xiaolei ZhuDepartment of Neurology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, PR China.
Nanjing University of Chinese Medicine · CNNanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synaptic loss induced by beta-amyloid (Aβ) plays a critical role in the pathophysiology of Alzheimer's disease (AD), but the mechanisms underlying this process remain unknown. In this study, we found that oridonin (Ori) rescued synaptic loss induced by Aβ1-42 in vivo and in vitro and attenuated the alterations in dendritic structure and spine density observed in the hippocampus of AD mice. In addition, Ori increased the expression of PSD-95 and synaptophysin and promoted mitochondrial activity in the synaptosomes of AD mice. Ori also activated the BDNF/TrkB/CREB signaling pathway in the hippocampus of AD mice. Furthermore, in the Morris water maze test, Ori reduced latency and searching distance and increased the number of platform crosses in AD mice. These data suggest that Ori might prevent synaptic loss and improve behavioral symptoms in Aβ1-42-induced AD mice.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrain-Derived Neurotrophic FactorCognition DisordersCyclic AMP Response Element-Binding ProteinDendritic SpinesDisks Large Homolog 4 ProteinDiterpenes, KauraneGuanylate KinasesHippocampusHumansMaleMembrane ProteinsMice, Inbred C57BLMitochondriaAmyloid beta-PeptidesBrain-Derived Neurotrophic FactorCyclic AMP Response Element-Binding ProteinDisks Large Homolog 4 ProteinDiterpenes, KauraneDlg4 protein, mouseGuanylate KinasesMembrane ProteinsoridoninReceptor, trkBSynaptophysin

Identifiers

PMID26974541
PMCPMC4790895
OpenAlexW2299031675

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.