Evidence mapPaperPMID 35255986Full record

ArticleTranslational neurodegeneration2022

Long-term hyperglycemia aggravates α-synuclein aggregation and dopaminergic neuronal loss in a Parkinson's disease mouse model.

Yi-Qing Lv, Lin Yuan, Yan Sun, Hao-Wen Dou, Ji-Hui Su, Zhi-Pan Hou, Jia-Yi Li, Wen Li

Open access · goldAbstract read
In one paragraph

Article in Translational neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 3 pooled it
8.8field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 3 syntheses or guidelines pooled it, 71 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 2 institutions in 2 countries.

Yi-Qing Lv *Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang, 110122, China.
Lin Yuan *Laboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang, 110122, China.
Yan SunLaboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang, 110122, China.
Hao-Wen DouLaboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang, 110122, China.
Ji-Hui SuLaboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang, 110122, China.
Zhi-Pan HouLaboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang, 110122, China.
Jia-Yi LiLaboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang, 110122, China. lijiayi@cmu.edu.cn.ORCID 0000-0002-7770-7376
Wen LiLaboratory of Research in Parkinson's Disease and Related Disorders, Health Sciences Institute, China Medical University, Shenyang, 110122, China. Wli87@cmu.edu.cn.ORCID 0000-0002-0383-0240
China Medical University · CNLund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGrowing evidence suggests an association between Parkinson's disease (PD) and diabetes mellitus (DM). At the cellular level, long-term elevated levels of glucose have been shown to lead to nigrostriatal degeneration in PD models. However, the underlying mechanism is still unclear. Previously, we have elucidated the potential of type 2 diabetes mellitus (T2DM) in facilitating PD progression, involving aggregation of both alpha-synuclein (α-syn) and islet amyloid polypeptide in the pancreatic and brain tissues. However, due to the complicated effect of insulin resistance on PD onset, the actual mechanism of hyperglycemia-induced dopaminergic degeneration remains unknown.

methodsWe employed the type 1 diabetes mellitus (T1DM) model induced by streptozotocin (STZ) injection in a transgenic mouse line (BAC-α-syn-GFP) overexpressing human α-syn, to investigate the direct effect of elevated blood glucose on nigrostriatal degeneration.

resultsSTZ treatment induced more severe pathological alterations in the pancreatic islets and T1DM symptoms in α-syn-overexpressing mice than in wild-type mice, at one month and three months after STZ injections. Behavioral tests evaluating motor performance confirmed the nigrostriatal degeneration. Furthermore, there was a marked decrease in dopaminergic profiles and an increase of α-syn accumulation and Serine 129 (S129) phosphorylation in STZ-treated α-syn mice compared with the vehicle-treated mice. In addition, more severe neuroinflammation was observed in the brains of the STZ-treated α-syn mice.

conclusionOur results solidify the potential link between DM and PD, providing insights into how hyperglycemia induces nigrostriatal degeneration and contributes to pathogenic mechanisms in PD.

Indexed as

Diabetes Mellitus, Type 1Diabetes Mellitus, Type 2HyperglycemiaParkinson Diseasealpha-SynucleinAnimalsDisease Models, AnimalDopamineMiceMice, Transgenicalpha-SynucleinDopamineDiabetes mellitusHyperglycemiaNeurodegenerationNeuroinflammationParkinson’s disease

Identifiers

PMID35255986
PMCPMC8900445
OpenAlexW4220880286

What Socratic holds

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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 Socratic graph.