Evidence map›Paper›PMID 25470026›Full record

ArticleInternational journal of molecular sciences2014

TGF-β1 protection against Aβ1-42-induced neuroinflammation and neurodegeneration in rats.

Wei-Xing Shen, Jia-Hui Chen, Jian-Hua Lu, Yu-Ping Peng, Yi-Hua Qiu

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. 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
3.1field-weighted citation impact, top 8% 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, 56 citations in OpenAlex.

  1. Article
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  16. Physostigmine Restores Impaired Autophagy in the Rat Hippocampus after Surgery Stress and LPS Treatment.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018
    Article
  17. 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

5 authors at 2 institutions in 1 country.

Wei-Xing ShenSchool of Biological & Basic Medical Sciences, Soochow University, 199 Renai Road, Suzhou 215123, China. swx@ntu.edu.cn.
Jia-Hui ChenDepartment of Physiology, School of Medicine, Nantong University, 19 Qixiu Road, Nantong 226001, China. liuzhan8301@163.com.
Jian-Hua LuDepartment of Physiology, School of Medicine, Nantong University, 19 Qixiu Road, Nantong 226001, China. ljhua@ntu.edu.cn.
Yu-Ping PengDepartment of Physiology, School of Medicine, Nantong University, 19 Qixiu Road, Nantong 226001, China. yppeng@ntu.edu.cn.
Yi-Hua QiuDepartment of Physiology, School of Medicine, Nantong University, 19 Qixiu Road, Nantong 226001, China. yhqiu@ntu.edu.cn.
Nantong University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor (TGF)-β1, a cytokine that can be expressed in the brain, is a key regulator of the brain's responses to injury and inflammation. Alzheimer's disease (AD), the most common neurodegenerative disorder, involves inflammatory processes in the brain in addition to the hallmarks, amyloid-β (Aβ) plaques and neurofibrillary tangles. Recently, we have shown that T-helper (Th) 17 cells, a subpopulation of CD4+ T-cells with high proinflammation, also participate in the brain inflammatory process of AD. However, it is poorly known whether TGF-β1 ameliorates the lymphocyte-mediated neuroinflammation and, thereby, alleviates neurodegeneration in AD. Herein, we administered TGF-β1 via the intracerebroventricle (ICV) in AD model rats, by Aβ1-42 injection in both sides of the hippocampus, to show the neuroprotection of TGF-β1. The TGF-β1 administration after the Aβ1-42 injection ameliorated cognitive deficit and neuronal loss and apoptosis, reduced amyloid precursor protein (APP) expression, elevated protein phosphatase (PP)2A expression, attenuated glial activation and alleviated the imbalance of the pro-inflammatory/anti-inflammatory responses of T-lymphocytes, compared to the Aβ1-42 injection alone. These findings demonstrate that TGF-β1 provides protection against AD neurodegeneration and suggest that the TGF-β1 neuroprotection is implemented by the alleviation of glial and T-cell-mediated neuroinflammation.

Indexed as

Amyloid beta-PeptidesAnimalsBrainCognitionCytokinesDown-RegulationHippocampusHypothalamusInflammationInflammation MediatorsNerve DegenerationNeuronsNeuroprotective AgentsPeptide FragmentsRats, Sprague-DawleyT-LymphocytesAmyloid beta-Peptidesamyloid beta-protein (1-42)CytokinesInflammation MediatorsNeuroprotective AgentsPeptide FragmentsTransforming Growth Factor beta1

Identifiers

PMID25470026
PMCPMC4284696
OpenAlexW2024094300

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.