Evidence map›Paper›PMID 30542451›Full record

ArticleExperimental and therapeutic medicine2018

Ellagic acid ameliorates learning and memory impairment in APP/PS1 transgenic mice via inhibition of β-amyloid production and tau hyperphosphorylation.

Lili Zhong, Hong Liu, Weijia Zhang, Xu Liu, Bo Jiang, Hongxin Fei, Zhongren Sun

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  8. The potential ofFrontiers in pharmacology · 2024
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  11. Antioxidants (Basel, Switzerland) · 2023
    Article
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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 3 institutions in 1 country.

Lili ZhongDepartment of Pathology, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150001, P.R. China.
Hong LiuPostdoctoral Program, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150040, P.R. China.
Weijia ZhangSecond Department of Orthopedic Surgery, Harbin First Hospital, Harbin, Heilongjiang 150010, P.R. China.
Xu LiuExperimental Center, School of Basic Medical Sciences, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150040, P.R. China.
Bo JiangDrug Safety Evaluation Center, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150040, P.R. China.
Hongxin FeiDepartment of Pathology, Qiqihar Medical University, Qiqihar, Heilongjiang 161006, P.R. China.
Zhongren SunKey Laboratory of Acupuncture Clinical Neurobiology (Encephalopathy), Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150040, P.R. China.
Heilongjiang University of Chinese Medicine · CNFirst Affiliated Hospital of Heilongjiang University of Chinese Medicine · CNQiqihar Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-amyloid (Aβ) aggregation and tau hyperphosphorylation are considered to be the primary pathological hallmarks of Alzheimer's disease (AD). Targeted inhibition of these pathological processes may provide effective treatments for AD. Accumulating evidence has demonstrated that ellagic acid (EA) exerts neuroprotective effects in several diseases. The present study investigated the effects of EA on AD-associated learning and memory deficits on APP/PS1 double transgenic mice and the underlying mechanisms. APP/PS1 mice or wild-type C57BL/6 mice were intragastrically administered EA (50 mg/kg/day) or vehicle for 60 consecutive days. The learning and memory abilities of mice were investigated using the Morris water maze test. Hippocampal regions were examined for the presence of amyloid plaques, neuronal apoptosis and tau phosphorylation. Expression levels of APP, Aβ, RAC-αserine/threonine-protein kinase and glycogen synthase kinase (GSK)3β in the hippocampus were determined by western blot analysis and ELISA. The results demonstrated that EA treatment ameliorated spatial learning and memory impairment in APP/PS1 mice and significantly reduced neuronal apoptosis and Aβ deposition in the hippocampus (P<0.05 and P<0.01). In addition, EA significantly inhibited the hyperphosphorylation of tau and significantly decreased the activity of glycogen synthase kinase (GSK)3β (P<0.01), which is involved in tau phosphorylation. Overall, these findings indicated that the beneficial effects of EA on AD-associated cognitive impairments may be attributed to the inhibition of Aβ production and tau hyperphosphorylation, and its beneficial action may be mediated in part, by the RAC-α serine/threonine-protein kinase/GSK3β signaling pathway.

Indexed as

Alzheimer's diseasecognitive impairmentellagic acidglycogen synthase kinase 3βtau hyperphosphorylation

Identifiers

PMID30542451
PMCPMC6257515
OpenAlexW2896300919

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.