Evidence map›Paper›PMID 33027640›Full record

ArticleNeuron2020

Rescuing Over-activated Microglia Restores Cognitive Performance in Juvenile Animals of the Dp(16) Mouse Model of Down Syndrome.

Bruno Pinto, Giovanni Morelli, Mohit Rastogi, Annalisa Savardi, Amos Fumagalli, Andrea Petretto, Martina Bartolucci, Emilio Varea, Tiziano Catelani, Andrea Contestabile and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
8.0field-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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Bruno PintoBIO@SNS, Scuola Normale Superiore, Piazza dei Cavalieri 7, 56126 Pisa, Italy; Brain Development and Disease Laboratory, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy.
Giovanni MorelliBrain Development and Disease Laboratory, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy.
Mohit RastogiBrain Development and Disease Laboratory, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy.
Annalisa SavardiBrain Development and Disease Laboratory, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy.
Amos FumagalliBrain Development and Disease Laboratory, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy.
Andrea PetrettoCore Facilities - Clinical Proteomics and Metabolomics, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
Martina BartolucciCore Facilities - Clinical Proteomics and Metabolomics, IRCCS Istituto Giannina Gaslini, Genoa, Italy.
Emilio VareaCellular Biology Department, University of Valencia, Valencia, Spain.
Tiziano CatelaniElectron Microscopy Facility, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy.
Andrea ContestabileBrain Development and Disease Laboratory, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy.
Laura E PerliniBrain Development and Disease Laboratory, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy.
Laura CanceddaBrain Development and Disease Laboratory, Istituto Italiano di Tecnologia, via Morego 30, 16163 Genova, Italy; Dulbecco Telethon Institute, Rome, Italy. Electronic address: laura.cancedda@iit.it.
Italian Institute of Technology · ITIstituto Giannina Gaslini · ITScuola Normale Superiore · ITUniversitat de València · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are brain-resident immune cells and regulate mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by a supernumerary chromosome 21, containing also genes related to the immune system. In the hippocampus of the Dp(16) mouse model of DS and DS individuals, we found activated microglia, as assessed by their morphology; activation markers; and, for DS mice, electrophysiological profile. Accordingly, we found increased pro-inflammatory cytokine levels and altered interferon signaling in Dp(16) hippocampi. DS mice also showed decreased spine density and activity of hippocampal neurons and hippocampus-dependent cognitive behavioral deficits. Depletion of defective microglia or treatment with a commonly used anti-inflammatory drug rescued the neuronal spine and activity impairments and cognitive deficits in juvenile Dp(16) mice. Our results suggest an involvement of microglia in Dp(16)-mouse cognitive deficits and identify a new potential therapeutic approach for cognitive disabilities in DS individuals.

Indexed as

Disease Models, AnimalAdultAge FactorsAminopyridinesAnimalsAnti-Inflammatory Agents, Non-SteroidalCognitionDown SyndromeFemaleHippocampusHumansMaleMiceMice, Inbred C57BLMice, TransgenicMicrogliaAminopyridinesAnti-Inflammatory Agents, Non-SteroidalpexidartinibPyrrolesacetaminophencognitive defectsdendritic spinesDown syndromeDp(16)microglianeurodevelopmental disordersneuroinflammationproteomicsTs65Dn

Identifiers

PMID33027640
PMCPMC7736620
OpenAlexW3091844202

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.