Evidence map›Paper›PMID 23866266›Full record

ReviewJournal of neuroinflammation2013

Down's syndrome, neuroinflammation, and Alzheimer neuropathogenesis.

Donna M Wilcock, W Sue T Griffin

Abstract readReview
In one paragraph

Review in Journal of neuroinflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

130 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Review
  6. Review
  7. Article
  8. 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
  9. Vertebrate and Invertebrate Animal Models for the Study of Down Syndrome.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Lipoprotein(a) levels in Down syndrome: A conundrum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Neuropathology of trisomy 21 mosaicism in a case with early-onset dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  20. Blood biomarkers in Down syndrome: Facilitating Alzheimer's disease detection and monitoring.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review

70 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

2 authors.

Donna M WilcockDepartment of Physiology, Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA.
W Sue T Griffin

Funding

THE APOE-APP AXIS IN ALZHEIMER PATHOGENESISP01AG012411 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI GRIFFIN, SUE TILTON · 1995 to 2020
$25.0M
Center for Biomedical Research Excellence in the Molecular Basis of Human DiseaseP20GM103486 · NIGMS · UNIVERSITY OF KENTUCKY · PI LOUIS HERSH, LOUIS HERSH LOUIS HERSH · 2012 to 2013
$4.2M
Vascular breakdown in Alzheimers Disease with cerebrovascular diseaseR01NS079637 · NINDS · UNIVERSITY OF KENTUCKY · PI WILCOCK, DONNA M · 2012 to 2016
$1.6M
NIA NIH HHS NIH/NIA AG12411NIGMS NIH HHS P20GM103486NINDS NIH HHS NS079637NINDS NIH HHS R01 NS079637
6 · The paper itself

Abstract

Down syndrome (DS) is the result of triplication of chromosome 21 (trisomy 21) and is the prevailing cause of mental retardation. In addition to the mental deficiencies and physical anomalies noted at birth, triplication of chromosome 21 gene products results in the neuropathological and cognitive changes of Alzheimer's disease (AD). Mapping of the gene that encodes the precursor protein (APP) of the β-amyloid (Aβ) present in the Aβ plaques in both AD and DS to chromosome 21 was strong evidence that this chromosome 21 gene product was a principal neuropathogenic culprit in AD as well as DS. The discovery of neuroinflammatory changes, including dramatic proliferation of activated glia overexpressing a chromosome 2 gene product--the pluripotent immune cytokine interleukin-1 (IL-1)--and a chromosome 21 gene product--S100B--in the brains of fetuses, neonates, and children with DS opened the possibility that early events in Alzheimer pathogenesis were driven by cytokines. The specific chromosome 21 gene products and the complexity of the mechanisms they engender that give rise to the neuroinflammatory responses noted in fetal development of the DS brain and their potential as accelerators of Alzheimer neuropathogenesis in DS are topics of this review, particularly as they relate to development and propagation of neuroinflammation, the consequences of which are recognized clinically and neuropathologically as Alzheimer's disease.

Indexed as

Alzheimer DiseaseChromosomes, Human, Pair 21Down SyndromeHumansInflammation

Identifiers

PMID23866266
PMCPMC3750399

What OpenQuestion holds

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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.