Evidence map›Paper›PMID 28870521›Full record

ReviewFree radical biology & medicine2018

Clinical aspects and biomarkers of Alzheimer's disease in Down syndrome.

Panagiotis Zis, Andre Strydom

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07047963 (Neuropsychological Evaluation in Intellectual Disability), which is not on this map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
10.4field-weighted citation impact, top 1% 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.

NCT07047963 not yet recruitingnot on this mapstarted 2025, after this paper: background citation

Neuropsychological Evaluation in Intellectual Disability

TypeobservationalSponsorCentral Hospital, Nancy, FranceRan2025 to 2026Enrolled40ConditionsDown Syndrome (Trisomy 21), Neuropsychology, Cognitive Aging, Alzheimer DiseaseArmsENDI (Neuropsychological Evaluation in Intellectual Disability)
3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
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  18. Further understanding the connection between Alzheimer's disease and Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020
    Review
  19. Article
  20. Review
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

2 authors at 2 institutions in 1 country.

Panagiotis ZisAcademic Department of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, UK.
Andre StrydomDivision of Psychiatry, University College London, London, UK; Department of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neurosciences, King's College London, London, UK; The LonDownS Consortium, London, UK. Electronic address: andre.strydom@kcl.ac.uk.
Sheffield Teaching Hospitals NHS Foundation Trust · GBUniversity College London · GB

Funding

Medical Research Council MR/R024901/1Wellcome Trust 098330
6 · The paper itself

Abstract

Alzheimer's disease (AD) may affect in excess of 90% of individuals with Down syndrome (DS) after age 60, due to duplication of the APP gene in trisomy of chromosome 21, with neuropathology that is comparable to Sporadic AD and Familial AD (FAD). Previous literature suggested some unique features in clinical presentation of dementia in DS (DSd), which might be due to diagnostic difficulties, or represent a real difference compared to SAD or FAD. We review current knowledge on clinical diagnosis and presentation of dementia in DS in comparison with FAD due to APP mutations and APP duplication. We suggest that the clinical presentation in DS (prominent memory decline and behavioral symptoms, and early development of myoclonus and seizures) are similar to the clinical features associated with APP mutations that is known to have an increased Aβ42/ Aβ40 ratio, and highlight the relative lack of vascular complications associated with cerebral amyloid angiopathy in DS in comparison with those rare individuals with FAD due to duplication APP. We consider the biomarker evidence associated with DS and DSd with reference to Aβ peptide levels and oxidative stress, and suggest future directions for research to explore the potential mechanisms associated with the clinical presentation of DSd.

Indexed as

MutationAlzheimer DiseaseBiomarkersDown SyndromeHumansBiomarkersAlzheimer's diseaseAPP mutationBiomarkersDown syndromeFamilial

Identifiers

PMID28870521
PMCPMC6451620
OpenAlexW2753376476

What OpenQuestion holds

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Registered trials

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.