Evidence map›Paper›PMID 32706757›Full record

ArticleAging2020

Minocycline inhibition of microglial rescues nigrostriatal dopaminergic neurodegeneration caused by mutant alpha-synuclein overexpression.

Yong Wang, Qian Wang, Ruobing Yu, Qi Zhang, Zhonghai Zhang, Haiying Li, Chao Ren, Rongli Yang, Haichen Niu

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Understanding the Molecular Basis of Miller-Dieker Syndrome.International journal of molecular sciences · 2025
    Review
  3. Review
  4. Review
  5. Article
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  10. Article
  11. Reduction of Lewy Body Pathology by Oral Cinnamon.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021
    Article
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 1 country.

Yong WangDepartment of Neurology, First Affiliated Hospital of Soochow University, Suzhou 215006, China.
Qian WangAffiliated First Clinical College of Xuzhou Medical University, Xuzhou 221004, China.
Ruobing YuDepartment of Genetics, Xuzhou Medical University, Xuzhou 221004, China.
Qi ZhangExperimental Animal Center, Xuzhou Medical University, Xuzhou 221004, China.
Zhonghai ZhangDeprtment of Physiology, Xuzhou Medical University, Xuzhou 221004, China.
Haiying LiDepartment of Pathology, Xuzhou Medical University, Xuzhou 221004, China.
Chao RenDepartment of Neurology, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai 264000, China.
Rongli YangAffiliated First Clinical College of Xuzhou Medical University, Xuzhou 221004, China.
Haichen NiuDepartment of Genetics, Xuzhou Medical University, Xuzhou 221004, China.
Xuzhou Medical College · CNFirst Affiliated Hospital of Soochow University · CNYuhuangding Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies indicate that mutant α-synuclein (mαSyn) is involved in the pathogenesis of Parkinson's disease (PD). The mαSyn expression leads to the loss of dopaminergic neurons in the substantia nigra (SN) and consequent motor dysfunctions. Additionally, studies found that PD was accompanied by extensive neuroinflammation of SN. However, it remains unclear as to whether microglia participate in the mαSyn pathology. This issue is addressed by using AAV-mα-Syn (A30P-A53T) to overexpress the human mαSyn in the SN in view of establishing the PD model. Subsequently, minocycline (Mino) was used to inhibit microglia activity, and an interleukin-1 receptor (IL-1R1) antagonist was used to hinder the IL-1R1 function. Finally, immunohistochemistry was used to analyze phosphorylated αSyn (Ser129) and TH-positive cells in the SN. Dopamine levels were analyzed by high performance liquid chromatography. mαSyn overexpression in the SN induced motor dysfunction, decreased striatal dopamine levels, and increased pathological αSyn 12 weeks after AAV injection. The data demonstrated that inhibiting microglial activation or hindering IL-1R1 reversed the persistent motor deficits, neurodegeneration of the nigrostriatal dopaminergic system, and development of Lewy body pathology caused by human mαSyn overexpression in the SN. Additionally, these findings indicate that neuroinflammation promotes the loss of neuronal cells.

Indexed as

alpha-SynucleinAnimalsBehavior, AnimalCorpus StriatumDopamineDopaminergic NeuronsHumansLewy BodiesMaleMiceMice, Inbred C57BLMicrogliaMinocyclineMotor ActivityMutationNerve Degenerationalpha-SynucleinDopamineIL1R1 protein, humanMinocyclineReceptors, Interleukin-1 Type ISNCA protein, humanIL-1βlewy-like pathologymicroglianeuroinflammationParkinson’s diseaseα-synuclein

Identifiers

PMID32706757
PMCPMC7425448
OpenAlexW3045119216

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.