Evidence map›Paper›PMID 34603007›Full record

ReviewFrontiers in aging neuroscience2021

Innate Immune System Activation and Neuroinflammation in Down Syndrome and Neurodegeneration: Therapeutic Targets or Partners?

Md Mahiuddin Ahmed, Noah R Johnson, Timothy D Boyd, Christina Coughlan, Heidi J Chial, Huntington Potter

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Observational
  5. Article
  6. Review
  7. Article
  8. 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. Risk of Alzheimer's disease in Down syndrome: Insights gained by multi-omics.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  13. Resistance and resilience to Alzheimer's disease in Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  14. Reversing intellectual disabilities in Down syndrome: Hopes or hypes?The Indian journal of medical research · 2025
    Article
  15. Review
  16. Blood biomarkers in Down syndrome: Facilitating Alzheimer's disease detection and monitoring.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  17. Review
  18. Article
  19. Article
  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

6 authors at 1 institution in 1 country.

Md Mahiuddin AhmedDepartment of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Noah R JohnsonDepartment of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Timothy D BoydDepartment of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Christina CoughlanDepartment of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Heidi J ChialDepartment of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Huntington PotterDepartment of Neurology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
University of Colorado Anschutz Medical Campus · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immune system activation and inflammation are associated with and may contribute to clinical outcomes in people with Down syndrome (DS), neurodegenerative diseases such as Alzheimer's disease (AD), and normal aging. In addition to serving as potential diagnostic biomarkers, innate immune system activation and inflammation may play a contributing or causal role in these conditions, leading to the hypothesis that effective therapies should seek to dampen their effects. However, recent intervention studies with the innate immune system activator granulocyte-macrophage colony-stimulating factor (GM-CSF) in animal models of DS, AD, and normal aging, and in an AD clinical trial suggest that activating the innate immune system and inflammation may instead be therapeutic. We consider evidence that DS, AD, and normal aging are accompanied by innate immune system activation and inflammation and discuss whether and when during the disease process it may be therapeutically beneficial to suppress or promote such activation.

Indexed as

Alzheimer’s diseaseamyloid-βapolipoprotein EDown syndromedrug repurposing and discoveryGM-CSF (granulocyte-macrophage colony-stimulating factor)inflammationinnate immune system

Identifiers

PMID34603007
PMCPMC8481947
OpenAlexW3200114640

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.