Evidence map›Paper›PMID 32517787›Full record

ArticleAlzheimer's research & therapy2020

Plasma transferrin and hemopexin are associated with altered Aβ uptake and cognitive decline in Alzheimer's disease pathology.

Azhaar Ashraf, Nicholas J Ashton, Pratishtha Chatterjee, Kathryn Goozee, Kaikai Shen, Jurgen Fripp, David Ames, Christopher Rowe, Colin L Masters, Victor Villemagne and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Alzheimer's research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. New Insights into Hemopexin-Binding to Hemin and Hemoglobin.International journal of molecular sciences · 2022
    Article
  12. Iron and Alzheimer's Disease: From Pathology to Imaging.Frontiers in human neuroscience · 2022
    Review
  13. Article
  14. Review
  15. Review
  16. Review
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  18. Article
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

14 authors at 6 institutions in 3 countries.

Azhaar AshrafDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Clinical Neuroscience Institute, King's College London, 5, Cutcombe Road, Denmark Hill Campus, London, SE5 9RX, UK.
Nicholas J AshtonInstitute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Institute Clinical Neuroscience Institute, King's College London, London, UK.
Pratishtha ChatterjeeSchool of Medical Sciences, Edith Cowan University, 270, Joondalup, WA, 6027, Australia.
Kathryn GoozeeKaRa Institute of Neurological Diseases, Macquarie Park, NSW, Australia.
Kaikai ShenAustralian E-Health Research Centre, CSIRO, Brisbane, Australia.
Jurgen FrippRapiscan Systems, St Leonards, Sydney, Australia.
David AmesAcademic Unit for Psychiatry of Old Age, St. George's Hospital, University of Melbourne, Victoria, VIC, Australia.
Christopher RoweDepartment of Molecular Imaging and Therapy, Austin Health, Heidelberg, VIC, Australia.
Colin L MastersThe Florey Institute, University of Melbourne, Parkville, VIC, Australia.
Victor VillemagneDepartment of Molecular Imaging and Therapy, Austin Health, Heidelberg, VIC, Australia.
Abdul HyeInstitute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Institute Clinical Neuroscience Institute, King's College London, London, UK.
Ralph N MartinsSchool of Medical Sciences, Edith Cowan University, 270, Joondalup, WA, 6027, Australia. ralph.martins@mq.edu.au.
Po-Wah SoDepartment of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Clinical Neuroscience Institute, King's College London, 5, Cutcombe Road, Denmark Hill Campus, London, SE5 9RX, UK. po-wah.so@kcl.ac.uk.ORCID 0000-0003-3449-8532
AIBL
King's College London · GBAustin Health · AUEdith Cowan University · AUThe University of Melbourne · AUCommonwealth Scientific and Industrial Research Organisation · AUThe University of Western Australia · AU

Funding

Biotechnology and Biological Sciences Research Council
6 · The paper itself

Abstract

backgroundHeme and iron homeostasis is perturbed in Alzheimer's disease (AD); therefore, the aim of the study was to examine the levels and association of heme with iron-binding plasma proteins in cognitively normal (CN), mild cognitive impairment (MCI), and AD individuals from the Australian Imaging, Biomarker and Lifestyle Flagship Study of Ageing (AIBL) and Kerr Anglican Retirement Village Initiative in Ageing Health (KARVIAH) cohorts.

methodsNon-targeted proteomic analysis by high-resolution mass spectrometry was performed to quantify relative protein abundances in plasma samples from 144 CN individuals from the AIBL and 94 CN from KARVIAH cohorts and 21 MCI and 25 AD from AIBL cohort. ANCOVA models were utilized to assess the differences in plasma proteins implicated in heme/iron metabolism, while multiple regression modeling (and partial correlation) was performed to examine the association between heme and iron proteins, structural neuroimaging, and cognitive measures.

resultsOf the plasma proteins implicated in iron and heme metabolism, hemoglobin subunit β (p = 0.001) was significantly increased in AD compared to CN individuals. Multiple regression modeling adjusted for age, sex, APOEε4 genotype, and disease status in the AIBL cohort revealed lower levels of transferrin but higher levels of hemopexin associated with augmented brain amyloid deposition. Meanwhile, transferrin was positively associated with hippocampal volume and MMSE performance, and hemopexin was negatively associated with CDR scores. Partial correlation analysis revealed lack of significant associations between heme/iron proteins in the CN individuals progressing to cognitive impairment.

conclusionsIn conclusion, heme and iron dyshomeostasis appears to be a feature of AD. The causal relationship between heme/iron metabolism and AD warrants further investigation.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesAustraliaHemopexinHumansProteomicsTransferrinAmyloid beta-PeptidesHemopexinTransferrinAlzheimer’s diseaseCognitive impairmentCognitively normalHemeHemoglobinIronMild cognitive impairmentProteomicsTransferrin

Identifiers

PMID32517787
PMCPMC7285604
OpenAlexW3033284966

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.