Evidence map›Paper›PMID 26846170›Full record

ArticleBMC neurology2016

Atorvastatin in improvement of cognitive impairments caused by amyloid β in mice: involvement of inflammatory reaction.

Liandong Zhao, Tingting Chen, Chonghui Wang, Guoxi Li, Wenhui Zhi, Jun Yin, Qi Wan, Ling Chen

Open access · goldAbstract read
In one paragraph

Article in BMC neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Simvastatin rescues cognitive impairment in an AβNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  10. Lipids and Alzheimer's Disease.International journal of molecular sciences · 2020
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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 3 institutions in 1 country.

Liandong ZhaoDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu, 210029, China.
Tingting ChenDepartment of Physiology, Nanjing Medical University, Nanjing, 210029, China.
Chonghui WangDepartment of Physiology, Nanjing Medical University, Nanjing, 210029, China.
Guoxi LiDepartment of Physiology, Nanjing Medical University, Nanjing, 210029, China.
Wenhui ZhiDepartment of Physiology, Nanjing Medical University, Nanjing, 210029, China.
Jun YinDepartment of Physiology, Nanjing Medical University, Nanjing, 210029, China.
Qi WanDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu, 210029, China. qi_wan@126.com.
Ling ChenDepartment of Physiology, Nanjing Medical University, Nanjing, 210029, China. lingchen@njmu.edu.cn.
Nanjing Medical University · CNJiangsu Province Hospital · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe production of inflammatory cytokines resulting from amyloid β (Aβ) is associated with the initiation of Alzheimer's disease (AD). Atorvastatin (ATV) has been reported to improve AD, however, it is unclear how the anti-inflammatory mechanism is linked with its protection against the impairment of spatial cognitive function in AD. The present study was designed to explore what mechanism was possibly involved in the anti-inflammatory pathway in regard to the ATV treatment of AD.

methodsWe used an AD model induced by the administration of Aβ(25-35) in male C57BL/6 mice and an in vitro culture system to study the protective effects of ATV on the spatial cognitive deficits, hippocampal long-term potentiation (LTP) impairment and inflammatory reaction.

resultsThe intragastric administration of ATV (5 mg/kg) in Aβ(25-35)-treated mice significantly ameliorated the spatial cognitive deficits and prevented the LTP impairment in hippocampal CA1. The increased Iba-1 positive cells and inflammatory components in the hippocampus were reduced after the ATV treatment. The anti-inflammatory and LTP protection of ATV were abolished using the replenishment of farnesyl pyrophosphate by the administration of farnesol (FOH). The hippocampal slices culture showed Aβ(25-35)-induced neurotoxicity in the absence of the presence of ATV. Treatment with ATV (0.5, 1, 2.5 μmol/L) dose-dependently prevented the cell damage in hippocampus induced by Aβ25-35.

conclusionThe administration of ATV ameliorated the cognitive deficits, depressed the inflammatory responses, improved the LTP impairment, and prevents Aβ25-35-induced neurotoxicity in cultured hippocampal neurons. These protective functions of ATV involved the pathway of reducing farnesyl pyrophosphate (FPP).

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAtorvastatinCytokinesDisease Models, AnimalHippocampusHydroxymethylglutaryl-CoA Reductase InhibitorsLong-Term PotentiationMaze LearningMice, Inbred C57BLAmyloid beta-PeptidesAtorvastatinCytokinesHydroxymethylglutaryl-CoA Reductase Inhibitors

Identifiers

PMID26846170
PMCPMC4743318
OpenAlexW2271163593

What OpenQuestion holds

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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.