Evidence map›Paper›PMID 39183331›Full record

ArticleMolecular neurodegeneration2024

Pathological characteristics of axons and alterations of proteomic and lipidomic profiles in midbrain dopaminergic neurodegeneration induced by WDR45-deficiency.

Panpan Wang, Yaping Shao, Murad Al-Nusaif, Jun Zhang, Huijia Yang, Yuting Yang, Kunhyok Kim, Song Li, Cong Liu, Huaibin Cai and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurodegeneration, 2024. 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
–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

11 citing papers in PubMed.

  1. Functional Homology of WIPI4 and Atg18 EnablesInternational journal of molecular sciences · 2026
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  2. Article
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  5. Article
  6. Article
  7. Review
  8. Mutation inFrontiers in neuroscience · 2025
    Article
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  10. Review
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Panpan WangLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China.
Yaping ShaoLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China.
Murad Al-NusaifLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China.
Jun ZhangLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China.
Huijia YangLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China.
Yuting YangLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China.
Kunhyok KimLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China.
Song LiLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China.
Cong LiuInterdisciplinary Research Center On Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China.
Huaibin CaiTransgenic Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, 20892, USA.
Weidong LeLiaoning Provincial Key Laboratory for Research On the Pathogenic Mechanisms of Neurological Diseases, The First Affiliated Hospital, Dalian Medical University, Dalian, 116021, China. wdle@sibs.ac.cn.ORCID 0000-0001-7459-2705

Funding

NIA NIH HHS AG000928NIA NIH HHS AG000944
6 · The paper itself

Abstract

backgroundAlthough WD repeat domain 45 (WDR45) mutations have been linked to

methodsTo investigate the impacts of WDR45 dysfunction on mouse behaviors and DAergic neurons, we developed a mouse model in which WDR45 was conditionally knocked out in the midbrain DAergic neurons (WDR45

resultsOur study of WDR45

conclusionsIn this study, we uncovered the molecular mechanisms underlying the contribution of WDR45 deficiency to axonal degeneration, which involves complex relationships between phospholipid metabolism, autophagy, and tubular ER. These findings greatly advance our understanding of the fundamental molecular mechanisms driving axonal degeneration and may provide a foundation for developing novel mechanistically based therapeutic interventions for BPAN and other neurodegenerative diseases.

Indexed as

AxonsDopaminergic NeuronsLipidomicsMesencephalonMice, KnockoutProteomicsAnimalsCarrier ProteinsDisease Models, AnimalMiceNerve DegenerationNeurodegenerative DiseasesCarrier ProteinsWdr45 protein, mouseAutophagyAxonal degenerationLpcat1Phospholipid metabolismTubular ERWDR45

Identifiers

PMID39183331
PMCPMC11346282

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.