Evidence map›Paper›PMID 28349199›Full record

ArticleActa neuropathologica2017

Amyloid-β accumulation in the CNS in human growth hormone recipients in the UK.

Diane L Ritchie, Peter Adlard, Alexander H Peden, Suzanne Lowrie, Margaret Le Grice, Kimberley Burns, Rosemary J Jackson, Helen Yull, Michael J Keogh, Wei Wei and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
6.2field-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

63 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Clinical Management of Cerebral Amyloid Angiopathy.Journal of clinical medicine · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 1 country.

Diane L RitchieNational CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, Deanery of Clinical Medicine, University of Edinburgh, Edinburgh, EH4 2XU, UK. diane.ritchie@ed.ac.uk.ORCID 0000-0002-3614-9638
Peter AdlardUCL Great Ormond Street Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Alexander H PedenNational CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, Deanery of Clinical Medicine, University of Edinburgh, Edinburgh, EH4 2XU, UK.
Suzanne LowrieNational CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, Deanery of Clinical Medicine, University of Edinburgh, Edinburgh, EH4 2XU, UK.
Margaret Le GriceNational CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, Deanery of Clinical Medicine, University of Edinburgh, Edinburgh, EH4 2XU, UK.
Kimberley BurnsNational CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, Deanery of Clinical Medicine, University of Edinburgh, Edinburgh, EH4 2XU, UK.
Rosemary J JacksonCentre for Cognitive and Neural Systems, University of Edinburgh, 1 George Square, Edinburgh, EH8 9JZ, UK.
Helen YullNational CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, Deanery of Clinical Medicine, University of Edinburgh, Edinburgh, EH4 2XU, UK.
Michael J KeoghDepartment of Clinical Neurosciences, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0QQ, UK.
Wei WeiMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0XY, UK.
Patrick F ChinneryMRC Mitochondrial Biology Unit, University of Cambridge, Cambridge Biomedical Campus, Cambridge, CB2 0XY, UK.
Mark W HeadNational CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, Deanery of Clinical Medicine, University of Edinburgh, Edinburgh, EH4 2XU, UK.
James W IronsideNational CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, Deanery of Clinical Medicine, University of Edinburgh, Edinburgh, EH4 2XU, UK.
University of Edinburgh · GBUniversity of Cambridge · GBGreat Ormond Street Hospital · GB

Funding

Medical Research Council G0400074Medical Research Council G0502157Medical Research Council G0600953Medical Research Council G0601943Medical Research Council G0900580Medical Research Council G0900652Medical Research Council G1100540Medical Research Council MC_UP_1501/2Medical Research Council MR/L016400/1Wellcome Trust
6 · The paper itself

Abstract

Human-to-human transmission of Creutzfeldt-Jakob disease (CJD) has occurred through medical procedures resulting in iatrogenic CJD (iCJD). One of the commonest causes of iCJD was the use of human pituitary-derived growth hormone (hGH) to treat primary or secondary growth hormone deficiency. As part of a comprehensive tissue-based analysis of the largest cohort yet collected (35 cases) of UK hGH-iCJD cases, we describe the clinicopathological phenotype of hGH-iCJD in the UK. In the 33/35 hGH-iCJD cases with sufficient paraffin-embedded tissue for full pathological examination, we report the accumulation of the amyloid beta (Aβ) protein associated with Alzheimer's disease (AD) in the brains and cerebral blood vessels in 18/33 hGH-iCJD patients and for the first time in 5/12 hGH recipients who died from causes other than CJD. Aβ accumulation was markedly less prevalent in age-matched patients who died from sporadic CJD and variant CJD. These results are consistent with the hypothesis that Aβ, which can accumulate in the pituitary gland, was present in the inoculated hGH preparations and had a seeding effect in the brains of around 50% of all hGH recipients, producing an AD-like neuropathology and cerebral amyloid angiopathy (CAA), regardless of whether CJD neuropathology had occurred. These findings indicate that Aβ seeding can occur independently and in the absence of the abnormal prion protein in the human brain. Our findings provide further evidence for the prion-like seeding properties of Aβ and give insights into the possibility of iatrogenic transmission of AD and CAA.

Indexed as

AdolescentAdultAmyloid beta-PeptidesAmyloid beta-Protein PrecursorApolipoproteins ECentral Nervous SystemCohort StudiesCreutzfeldt-Jakob SyndromeDNA-Binding ProteinsExome SequencingFemaleHuman Growth HormoneHumansMaleMiddle AgedPrion ProteinsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorApolipoproteins EDNA-Binding ProteinsHuman Growth HormonePrion ProteinsTARDBP protein, humantau ProteinsAmyloid βCerebral amyloid angiopathyHuman growth hormoneIatrogenic Creutzfeldt–Jakob diseaseNeuropathologyPrion protein

Identifiers

PMID28349199
PMCPMC5508038
OpenAlexW2598800417

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.