Evidence map›Paper›PMID 29793416›Full record

ArticleCNS & neurological disorders drug targets2018

Oleanolic Acid Ameliorates Aβ25-35 Injection-induced Memory Deficit in Alzheimer's Disease Model Rats by Maintaining Synaptic Plasticity.

Kai Wang, Weiming Sun, Linlin Zhang, Wei Guo, Jiachun Xu, Shuang Liu, Zhen Zhou, Yulian Zhang

Open access · greenAbstract read
In one paragraph

Article in CNS & neurological disorders drug targets, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 45 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

8 authors at 1 institution in 1 country.

Kai WangGraduate Institutes, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
Weiming SunGraduate Institutes, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
Linlin ZhangDepartment of Neurology, the Second Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, Tianjin, 300150, China.
Wei GuoDepartment of Neurology, the Second Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, Tianjin, 300150, China.
Jiachun XuGraduate Institutes, Tianjin University of Traditional Chinese Medicine, Tianjin, 300193, China.
Shuang LiuDepartment of Neurology, the Second Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, Tianjin, 300150, China.
Zhen ZhouDepartment of Neurology, the Second Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, Tianjin, 300150, China.
Yulian ZhangDepartment of Neurology, the Second Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, Tianjin, 300150, China.
Tianjin University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbnormal amyloid β (Aβ) accumulation and deposition in the hippocampus is an essential process in Alzheimer's disease (AD).

objectiveTo investigate whether Oleanolic acid (OA) could improve memory deficit in AD model and its possible mechanism.

methodsForty-five SD rats were randomly divided into sham operation group, model group, and OA group. AD models by injection of Aβ25-35 were built. Morris water maze (MWM) was applied to investigate learning and memory, transmission electron microscope (TEM) to observe the ultrastructure of synapse, western blot to the proteins, electrophysiology for long-term potentiation (LTP), and Ca2+ concentration in synapse was also measured.

resultsThe latency time in model group was significantly longer than that in sham operation group (P=0.0001); while it was significantly shorter in the OA group than that in model group (P=0.0001); compared with model group, the times of cross-platform in OA group significantly increased (P=0.0001). TEM results showed OA could alleviate neuron damage and synapses changes induced by Aβ25-35. The expressions of CaMKII, PKC, NMDAR2B, BDNF, TrkB, and CREB protein were significantly improved by OA (P=0.0001, 0.036, 0.041, 0.0001, 0.0001, 0.026, respectively) compared with that in model group; the concentration of Ca2+ was significantly lower in OA group (1.11±0.42) than that in model group (1.68±0.18); and the slope rate (P=0.0001) and amplitude (P=0.0001) of f- EPSP significantly increased in OA group.

conclusionThe present results support that OA could ameliorate Aβ-induced memory loss of AD rats by maintaining synaptic plasticity of the hippocampus.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntipsychotic AgentsAvoidance LearningCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Disease Models, AnimalElectric StimulationHippocampusLong-Term PotentiationMaleMaze LearningMemory DisordersMicroscopy, Electron, TransmissionOleanolic AcidAmyloid beta-Peptidesamyloid beta-protein (25-35)Antipsychotic AgentsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2NR2B NMDA receptorOleanolic AcidPeptide FragmentsProtein Kinase CReceptors, N-Methyl-D-AspartateAlzheimer's diseaseAβCa2+long-term potentiationOleanolic acidsynaptic plasticity.

Identifiers

PMID29793416
PMCPMC6327117
OpenAlexW2804903936

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.