Evidence map›Paper›PMID 27578012›Full record

ArticleMolecular neurobiology2017

Expression of Iron Transporters and Pathological Hallmarks of Parkinson's and Alzheimer's Diseases in the Brain of Young, Adult, and Aged Rats.

Li-Na Lu, Zhong-Ming Qian, Ka-Chun Wu, Wing-Ho Yung, Ya Ke

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
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  7. Review
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  9. Article
  10. Review
  11. Genetic Markers of Postmortem Brain Iron.Journal of neurochemistry · 2025
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Iron Deposition in Parkinson's Disease: A Mini-Review.Cellular and molecular neurobiology · 2024
    Review
  17. Article
  18. Article
  19. Article
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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

5 authors at 2 institutions in 1 country.

Li-Na LuSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, SAR, China.
Zhong-Ming QianLaboratory of Neuropharmacology, School of Pharmacy, Fudan University, Shanghai, 201203, People's Republic of China. qianzhongming@fudan.edu.cn.
Ka-Chun WuSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, SAR, China.
Wing-Ho YungSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, SAR, China.
Ya KeSchool of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, SAR, China. yake@cuhk.edu.hk.
Chinese University of Hong Kong · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron accumulates progressively in the brain with age; however, the cause is unknown. We hypothesized that iron accumulation may be associated with the age-induced changes in the expression of iron metabolism proteins in the brain. Here, we systematically investigated iron content and the expression of two major iron importers, transferrin receptor 1 (TfR1) and divalent metal transporter (DMT1), two iron exporters, ferroportin 1 (Fpn1) and ceruloplasmin (CP), and hepcidin, along with the pathological hallmarks of Parkinson's (PD) and Alzheimer's diseases (AD) in the brain of young (3 months), adult (12 months), and aged (24 months) rats. We demonstrated that age has a region-specific effect on iron transport proteins along with iron content in the cortex, striatum, hippocampus, and substantia nigra. We also found an age-dependent increase in hyperphosphorylated tau, total beta-amyloid, and neurotoxic oligomeric aggregates in the cortex and hippocampus as well as an increase in α-synuclein and a decrease in tyrosine hydroxylase positive neurons in the substantia nigra. Our findings suggest that the age-dependent increase in brain iron may be partly due to the age-induced increase in DMT1 expression, rather than TfR1 and Fpn1 expression, and also imply that the increased brain iron is associated with expression of the pathological hallmarks of AD and PD.

Indexed as

AgingAlzheimer DiseaseAnimalsAstrocytesBrainCation Transport ProteinsHepcidinsIronMaleNeuronsParkinson DiseaseParkinsonian DisordersRats, Sprague-DawleyCation Transport ProteinsHepcidinsIronAgeBeta-amyloidHepcidinHyperphosphorylated tauIronIron uptake and release proteinsα-Synuclein

Identifiers

PMID27578012
OpenAlexW2510630146

What OpenQuestion holds

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Read underepoch 390

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.