Evidence map›Paper›PMID 40249399›Full record

ArticleEuropean journal of nutrition2025

Tissue zinc restoration alleviates the levodopa-induced dyskinesia via impeding ERK phosphorylation.

Meng-Di Zhang, Meng-Jie Gu, Qi Wang, Shuai-Mei Zhang, Wen-Xi Zhou, Shi-Biao Liu, Rong-Pei Liu, Chen-Ping Huang, Jian-Hong Zhu, Hong-Mei Wu

Abstract read
PubMed Publisher
In one paragraph

Article in European journal of nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Meng-Di Zhang *Institute of Nutrition and Diseases, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Meng-Jie Gu *Institute of Geriatric Neurology, Department of Neurology, the Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China.
Qi Wang *Institute of Nutrition and Diseases, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Shuai-Mei ZhangInstitute of Nutrition and Diseases, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Wen-Xi ZhouInstitute of Nutrition and Diseases, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Shi-Biao LiuInstitute of Nutrition and Diseases, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Rong-Pei LiuInstitute of Geriatric Neurology, Department of Neurology, the Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China.
Chen-Ping HuangInstitute of Nutrition and Diseases, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Jian-Hong ZhuInstitute of Nutrition and Diseases, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China. jhzhu@wmu.edu.cn.
Hong-Mei WuInstitute of Nutrition and Diseases, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China. hmwu@wmu.edu.cn.ORCID http://orcid.org/0009-0009-1120-6892

Funding

Wenzhou Medical University XZ2022001Wenzhou Municipal Science and Technology Bureau Y20190189Zhejiang Provincial Natural Science Foundation LGF21H260011
6 · The paper itself

Abstract

purposeLevodopa administration has been the standard therapy for Parkinson’s disease (PD) and prolonged treatment is associated with levodopa-induced dyskinesia (LID). This study aimed to identify the effects of zinc (Zn) supplements on LID and to explore the underlying mechanisms.

methodsMale C57BL/6J mice were injected with 6-OHDA at medial forebrain bundle, followed by daily levodopa injection to induce LID. The mice were supplemented with Zn of 0, 0.3, 1.2, or 2.4 mg/kg for 4 weeks.

resultsIn the LID mice, Zn supplements restored tissue Zn levels and alleviated global, forelimb, and orolingual abnormal involuntary movements (AIMs). Signaling pathway assessments showed that Zn supplements significantly reduced expressions of phosphorylated glutamate receptor 1 (p-GluR1) and phosphorylation levels of extracellular-signal-regulated kinase (p-ERK/ERK). Correlations between the AIMs score, p-ERK, and tissue Zn levels were established. In addition, Zn supplements reduced numbers of glial fibrillary acidic protein (GFAP) positive cells and compensatory tyrosine hydroxylase (TH) positive cells. These alleviating effects of Zn supplements were strictly regulated in a dose dependent manner.

conclusionAppropriate doses of Zn supplements alleviated AIMs in the LID mouse model, potentially via impeding ERK phosphorylation, inhibiting astrocyte activation, and attenuating striatal compensation of TH positive cells.

Indexed as

Dyskinesia, Drug-InducedExtracellular Signal-Regulated MAP KinasesLevodopaZincAnimalsDietary SupplementsDisease Models, AnimalMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLPhosphorylationTyrosine 3-MonooxygenaseExtracellular Signal-Regulated MAP KinasesLevodopaTyrosine 3-MonooxygenaseZincExtracellular-signal-regulated kinaseLevodopa-induced dyskinesiaParkinson’s diseaseZinc

Identifiers

PMID40249399

What OpenQuestion holds

Textmetadata
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.