Evidence map›Paper›PMID 30902060›Full record

ArticleAlzheimer's research & therapy2019

Plasma biomarkers for amyloid, tau, and cytokines in Down syndrome and sporadic Alzheimer's disease.

Carla M Startin, Nicholas J Ashton, Sarah Hamburg, Rosalyn Hithersay, Frances K Wiseman, Kin Y Mok, John Hardy, Alberto Lleó, Simon Lovestone, Lucilla Parnetti and 4 more

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

Article in Alzheimer's research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 6 pooled it
8.1field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 6 syntheses or guidelines pooled it, 90 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Blood-based biomarkers for Alzheimer's disease in Down syndrome: A systematic review and meta-analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Article
  9. Precision medicine for Alzheimer's disease in Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Targeting dysregulated CB1 receptors in a Down syndrome mouse model improves neurological outcomes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  14. Review
  15. Genome-wide association of tau neuroimaging and plasma biomarkers in adults with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  16. Article
  17. Blood biomarkers in Down syndrome: Facilitating Alzheimer's disease detection and monitoring.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  18. Review
  19. Article
  20. Plasma NT1-tau and AβAlzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    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 7 institutions in 5 countries.

Carla M StartinDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, 16 De Crespigny Park, London, SE5 8AF, UK. carla.startin.09@ucl.ac.uk.ORCID 0000-0001-9261-9924
Nicholas J AshtonMaurice Wohl Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Sarah HamburgDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, 16 De Crespigny Park, London, SE5 8AF, UK.
Rosalyn HithersayDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, 16 De Crespigny Park, London, SE5 8AF, UK.
Frances K WisemanThe LonDownS Consortium (London Down Syndrome Consortium), London, UK.
Kin Y MokThe LonDownS Consortium (London Down Syndrome Consortium), London, UK.
John HardyThe LonDownS Consortium (London Down Syndrome Consortium), London, UK.
Alberto LleóMemory Unit, Neurology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.
Simon LovestoneDepartment of Psychiatry, University of Oxford, Oxford, UK.
Lucilla ParnettiCentre for Memory Disturbances, Laboratory of Clinical Neurochemistry, Section of Neurology, Department of Medicine, University of Perugia, Perugia, Italy.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Abdul HyeMaurice Wohl Clinical Neuroscience, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
LonDownS Consortium
André StrydomDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, 16 De Crespigny Park, London, SE5 8AF, UK.
King's College London · GBUniversity College London · GBHong Kong University of Science and Technology · HKHospital de Sant Pau · ESSahlgrenska University Hospital · SEUniversity of Oxford · GBUniversity of Perugia · IT

Funding

Medical Research Council G0701075Medical Research Council G0901254Medical Research Council MR/K01417X/1Medical Research Council MR/L501542/1Medical Research Council MR/N026004/1Medical Research Council MR/R024901/1Medical Research Council MR/S011277/1Parkinson's UK G-0907Wellcome Trust 098330/Z/12/Z
6 · The paper itself

Abstract

backgroundDown syndrome (DS), caused by chromosome 21 trisomy, is associated with an ultra-high risk of dementia due to Alzheimer's disease (AD), driven by amyloid precursor protein (APP) gene triplication. Understanding relevant molecular differences between those with DS, those with sporadic AD (sAD) without DS, and controls will aid in understanding AD development in DS. We explored group differences in plasma concentrations of amyloid-β peptides and tau (as their accumulation is a characteristic feature of AD) and cytokines (as the inflammatory response has been implicated in AD development, and immune dysfunction is common in DS).

methodsWe used ultrasensitive assays to compare plasma concentrations of the amyloid-β peptides Aβ

resultsAβ

conclusionsConcentrations of Aβ

Indexed as

AdultAgedAlzheimer DiseaseAmyloid beta-PeptidesApolipoproteins EBiomarkersCytokinesDown SyndromeFemaleHumansMaleMiddle Agedtau ProteinsYoung AdultAmyloid beta-PeptidesApolipoproteins EBiomarkersCytokinesMAPT protein, humantau ProteinsAlzheimer’s diseaseAmyloidBiomarkerCytokinesDementiaDown syndromeInterleukin 1βPlasmaTau

Identifiers

PMID30902060
PMCPMC6429702
OpenAlexW2917093389

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.