Evidence map›Paper›PMID 36852451›Full record

ArticleCNS neuroscience & therapeutics2023

An imbalance of netrin-1 and DCC during nigral degeneration in experimental models and patients with Parkinson's disease.

Ye Hua, Wenjing Han, Linfeng Zhou, Jing Gao, Jifeng Zhao, Nanshan Song, Bin Hu, Qingyu Yao, Yumin Liu, Deen Xu and 2 more

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 11 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

12 authors at 3 institutions in 1 country.

Ye HuaDepartment of Neurology, Wuxi No.2 People's Hospital, Jiangnan University Medical Center, Wuxi, China.
Wenjing HanNeuroprotective Drug Discovery Center of Nanjing Medical University, Department of Pharmacology, Nanjing Medical University, Nanjing, China.
Linfeng ZhouNeuroprotective Drug Discovery Center of Nanjing Medical University, Department of Pharmacology, Nanjing Medical University, Nanjing, China.
Jing GaoNeuroprotective Drug Discovery Center of Nanjing Medical University, Department of Pharmacology, Nanjing Medical University, Nanjing, China.
Jifeng ZhaoNeuroprotective Drug Discovery Center of Nanjing Medical University, Department of Pharmacology, Nanjing Medical University, Nanjing, China.
Nanshan SongNeuroprotective Drug Discovery Center of Nanjing Medical University, Department of Pharmacology, Nanjing Medical University, Nanjing, China.
Bin HuDepartment of Clinical Laboratory, Wuxi No.2 People's Hospital, Jiangnan University Medical Center, Wuxi, China.
Qingyu YaoDepartment of Neurology, Wuxi No.2 People's Hospital, Jiangnan University Medical Center, Wuxi, China.
Yumin LiuDepartment of Neurology, Wuxi No.2 People's Hospital, Jiangnan University Medical Center, Wuxi, China.
Deen XuDepartment of Neurology, Wuxi No.2 People's Hospital, Jiangnan University Medical Center, Wuxi, China.
Yunnan LuDepartment of Neurology, Xishan People's Hospital of Wuxi City, Wuxi, China.
Yi FanNeuroprotective Drug Discovery Center of Nanjing Medical University, Department of Pharmacology, Nanjing Medical University, Nanjing, China.ORCID 0000-0003-1783-3220
Nanjing Medical University · CNJiangnan University · CNWuxi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsMultiple guidance cues, such as netrin-1 (NTN-1)/deleted in colorectal carcinoma (DCC), control the guidance of axons and help establish functional neural circuits during development. However, the function of these guidance molecules during the neurodegenerative process is unclear.

methodsTo access the alterations of NTN-1 and DCC during the onset and progression of PD, we first established two subacute and one chronic PD model. Then, we investigated the relationship between the NTN-1/DCC pathway and cell death in SH-SY5Y cells. Finally, we conducted correlation studies between plasma NTN-1 and parkinsonian symptoms in patients to understand how this pathway contributes to PD.

resultsWe found that the imbalance of NTN-1 and DCC was a common feature of nigral DA neuron injury in PD mouse models. We investigated that MPP+ inhibited NTN-1 expression and increased DCC expression in a concentration- and time-dependent manner. We further discovered a significant decrease in plasma NTN-1 levels and a positive correlation with UPDRS scores in PD patients.

conclusionOur findings confirmed the imbalance of NTN-1/DCC signaling during nigral degeneration in experimental PD models and found for the first time a correlation of plasma NTN-1 with PD symptoms in patients.

Indexed as

NeuroblastomaParkinson DiseaseAnimalsAxonsCells, CulturedDCC ReceptorHumansMiceNerve Growth FactorsNetrin-1Tumor Suppressor ProteinsDCC protein, humanDCC ReceptorNerve Growth FactorsNetrin-1Tumor Suppressor ProteinsDCCnetrin-1neurodegenerationParkinson's disease

Identifiers

PMID36852451
PMCPMC10324354
OpenAlexW4322617408

What OpenQuestion holds

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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.