Evidence map›Paper›PMID 27239286›Full record

ReviewF1000Research2016

Intracerebral haemorrhage in Down syndrome: protected or predisposed?

Lewis Buss, Elizabeth Fisher, John Hardy, Dean Nizetic, Jurgen Groet, Laura Pulford, André Strydom

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

Review in F1000Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Use of anti-amyloid-β monoclonal antibodies in persons with Down syndrome Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  3. Article
  4. Review
  5. Occurrence of mosaic Down syndrome and prevalence of co-occurring conditions in Medicaid enrolled adults, 2016-2019.American journal of medical genetics. Part C, Seminars in medical genetics · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Iron-responsive-like elements and neurodegenerative ferroptosis.Learning & memory (Cold Spring Harbor, N.Y.) · 2020
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. 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

7 authors at 3 institutions in 3 countries.

Lewis BussDivision of Psychiatry, University College London, London, UK; London Down Syndrome (LonDownS) Consortium, University College London, London, UK.
Elizabeth FisherInstitute of Neurology, University College London, London, UK; London Down Syndrome (LonDownS) Consortium, University College London, London, UK.
John HardyInstitute of Neurology, University College London, London, UK; London Down Syndrome (LonDownS) Consortium, University College London, London, UK.
Dean NizeticLee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore; Blizard Institute, Barts and the London School of Medicine, Queen Mary, University of London, London, UK; London Down Syndrome (LonDownS) Consortium, University College London, London, UK.
Jurgen GroetBlizard Institute, Barts and the London School of Medicine, Queen Mary, University of London, London, UK; London Down Syndrome (LonDownS) Consortium, University College London, London, UK.
Laura PulfordInstitute of Neurology, University College London, London, UK; London Down Syndrome (LonDownS) Consortium, University College London, London, UK.
André StrydomDivision of Psychiatry, University College London, London, UK; London Down Syndrome (LonDownS) Consortium, University College London, London, UK.
University College London · GBQueen Mary University of London · GBUniversidad de Londres · MX

Funding

Wellcome Trust
6 · The paper itself

Abstract

Down syndrome (DS), which arises from trisomy of chromosome 21, is associated with deposition of large amounts of amyloid within the central nervous system. Amyloid accumulates in two compartments: as plaques within the brain parenchyma and in vessel walls of the cerebral microvasculature. The parenchymal plaque amyloid is thought to result in an early onset Alzheimer's disease (AD) dementia, a phenomenon so common amongst people with DS that it could be considered a defining feature of the condition. The amyloid precursor protein ( APP) gene lies on chromosome 21 and its presence in three copies in DS is thought to largely drive the early onset AD. In contrast, intracerebral haemorrhage (ICH), the main clinical consequence of vascular amyloidosis, is a more poorly defined feature of DS. We review recent epidemiological data on stroke (including haemorrhagic stroke) in order to make comparisons with a rare form of familial AD due to duplication (i.e. having three copies) of the APP region on chromosome 21, here called 'dup-APP', which is associated with more frequent and severe ICH. We conclude that although people with DS are at increased risk of ICH, this is less common than in dup-APP, suggesting the presence of mechanisms that act protectively. We review these mechanisms and consider comparative research into DS and dup-APP that may yield further pathophysiological insight.

Indexed as

Alzheimer’s diseaseCerebral amyloid angiopathyDown syndromeIntracerebral haemorrhagetrisomy

Identifiers

PMID27239286
PMCPMC4870990
OpenAlexW2384007878

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.