Evidence map›Paper›PMID 26016857›Full record

ArticleJournal of neuroinflammation2015

Electroacupuncture remediates glial dysfunction and ameliorates neurodegeneration in the astrocytic α-synuclein mutant mouse model.

Jiahui Deng, E Lv, Jian Yang, Xiaoli Gong, Wenzhong Zhang, Xibin Liang, Jiazeng Wang, Jun Jia, Xiaomin Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 2 pooled it
2.0field-weighted citation impact, top 15% 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, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

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  15. Electroacupuncture Alleviates Ischemic Brain Injury by Inhibiting the miR-223/NLRP3 Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  16. Signal Transduction Pathways of Acupuncture for Treating Some Nervous System Diseases.Evidence-based complementary and alternative medicine : eCAM · 2019
    Review
  17. Review
  18. Article
  19. Article
  20. Acupuncture for acute stroke.The Cochrane database of systematic reviews · 2018
    Review
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

9 authors at 3 institutions in 2 countries.

Jiahui DengDepartments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China. jiahui_deng@sina.com.
E LvDepartments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China. shdlve@163.com.
Jian YangDepartments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China. kevinyangj@sina.com.
Xiaoli GongDepartments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China. gxl802@ccmu.edu.cn.
Wenzhong ZhangDepartments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China. zhagwenzhng@163.com.
Xibin LiangDepartment of Neurology and Neurological Sciences, Stanford University, Stanford, CA, 94305, USA. xliang1@stanford.edu.
Jiazeng WangDepartments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China. sdmcwjz@126.com.
Jun JiaDepartments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China. jiajun@ccmu.edu.cn.
Xiaomin WangDepartments of Neurobiology and Physiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, 100069, China. xmwang@ccmu.edu.cn.
Capital Medical University · CNChinese Institute for Brain Research · CNStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe acupuncture or electroacupuncture (EA) shows the therapeutic effect on various neurodegenerative diseases. This effect was thought to be partially achieved by its ability to alleviate existing neuroinflammation and glial dysfunction. In this study, we systematically investigated the effect of EA on abnormal neurochemical changes and motor symptoms in a mouse neurodegenerative disease model.

methodsThe transgenic mouse which expresses a mutant α-synuclein (α-syn) protein, A53T α-syn, in brain astrocytic cells was used. These mice exhibit extensive neuroinflammatory and motor phenotypes of neurodegenerative disorders. In this study, the effects of EA on these phenotypic changes were examined in these mice.

resultsEA improved the movement detected in multiple motor tests in A53T mutant mice. At the cellular level, EA significantly reduced the activation of microglia and prevented the loss of dopaminergic neurons in the midbrain and motor neurons in the spinal cord. At the molecular level, EA suppressed the abnormal elevation of proinflammatory factors (tumor necrosis factor-α and interleukin-1β) in the striatum and midbrain of A53T mice. In contrast, EA increased striatal and midbrain expression of a transcription factor, nuclear factor E2-related factor 2, and its downstream antioxidants (heme oxygenase-1 and glutamate-cysteine ligase modifier subunits).

conclusionsThese results suggest that EA possesses the ability to ameliorate mutant α-syn-induced motor abnormalities. This ability may be due to that EA enhances both anti-inflammatory and antioxidant activities and suppresses aberrant glial activation in the diseased sites of brains.

Indexed as

Neurodegenerative Diseasesalpha-SynucleinAnimalsAstrocytesCalcium-Binding ProteinsElectroacupunctureExploratory BehaviorGait Disorders, NeurologicGene Expression RegulationGlial Fibrillary Acidic ProteinGlutamate-Cysteine LigaseHeme Oxygenase-1Membrane ProteinsMiceMice, TransgenicMicrofilament ProteinsAif1 protein, mousealpha-SynucleinCalcium-Binding ProteinsGCLM protein, mouseGlial Fibrillary Acidic ProteinGlutamate-Cysteine LigaseHeme Oxygenase-1Hmox1 protein, mouseMembrane ProteinsMicrofilament ProteinsNfe2l2 protein, mouseNF-E2-Related Factor 2

Identifiers

PMID26016857
PMCPMC4449593
OpenAlexW1496327127

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.