Evidence map›Paper›PMID 34403733›Full record

ArticleBrain, behavior, and immunity2021

Novel microglia-mediated mechanisms underlying synaptic loss and cognitive impairment after traumatic brain injury.

Karen Krukowski, Amber Nolan, McKenna Becker, Katherine Picard, Nathalie Vernoux, Elma S Frias, Xi Feng, Marie-Eve Tremblay, Susanna Rosi

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

Article in Brain, behavior, and immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
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  15. Microglial plasticity across development mediates infantile amnesia.bioRxiv : the preprint server for biology · 2025
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  19. Impact Induces Phagocytic Defect in Reactive Microglia.bioRxiv : the preprint server for biology · 2025
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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

9 authors at 3 institutions in 2 countries.

Karen KrukowskiDepartment of Physical Therapy and Rehabilitation Science, University of California, San Francisco, CA, USA; Brain and Spinal Injury Center, University of California, San Francisco, CA, USA.
Amber NolanDepartment of Physical Therapy and Rehabilitation Science, University of California, San Francisco, CA, USA; Brain and Spinal Injury Center, University of California, San Francisco, CA, USA.
McKenna BeckerDepartment of Physical Therapy and Rehabilitation Science, University of California, San Francisco, CA, USA; Brain and Spinal Injury Center, University of California, San Francisco, CA, USA.
Katherine PicardAxe Neurosciences, CRCHU de Québec-Université Laval, Québec, QC, Canada.
Nathalie VernouxAxe Neurosciences, CRCHU de Québec-Université Laval, Québec, QC, Canada.
Elma S FriasDepartment of Physical Therapy and Rehabilitation Science, University of California, San Francisco, CA, USA; Brain and Spinal Injury Center, University of California, San Francisco, CA, USA; Department of Biomedical Sciences, University of California, San Francisco, CA, USA.
Xi FengDepartment of Physical Therapy and Rehabilitation Science, University of California, San Francisco, CA, USA; Brain and Spinal Injury Center, University of California, San Francisco, CA, USA.
Marie-Eve TremblayAxe Neurosciences, CRCHU de Québec-Université Laval, Québec, QC, Canada; Molecular Medicine Department, Université Laval, Québec, QC, Canada; Division of Medical Sciences, University of Victoria, Victoria, BC, Canada; Department of Biochemistry and Molecular Biology, The University of British Columbia, Vancouver, BC, Canada. Electronic address: evetremblay@uvic.ca.
Susanna RosiDepartment of Physical Therapy and Rehabilitation Science, University of California, San Francisco, CA, USA; Brain and Spinal Injury Center, University of California, San Francisco, CA, USA; Department of Biomedical Sciences, University of California, San Francisco, CA, USA; Department of Neurological Surgery, University of California, San Francisco, CA, USA; Weill Institute for Neuroscience, University of California San Francisco, CA, USA; Kavli Institute of Fundamental Neuroscience, University of California San Francisco, CA, USA. Electronic address: susanna.rosi@ucsf.edu.
University of California, San Francisco · USUniversité Laval · CAUniversity of British Columbia · CA

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MALLORY O JOHNSON · 1988 to 2026
$93.6M
Maximizing Opportunities for Research Excellence - Evaluation Training SupplementR25GM056847 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DUNCAN, D'ANNE S., SELLO, JASON K · 1998 to 2023
$14.1M
NRSA Training CoreTL1TR001871 · NCATS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KANAYA, ALKA M., SOMSOUK, MA · 2016 to 2025
$10.1M
Myeloid cells and radiation-induced memory deficits in rodent glioma model: sex and age effectsR01CA246722 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GUPTA, NALIN · 2020 to 2024
$1.8M
Aging exacerbates trauma-induced immune pathways and neuronal dysfunctionR01AG056770 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSI, SUSANNA · 2017 to 2021
$1.7M
Cortical Somatostatin Interneuron Dysfunction after Trauma: Role in Cognitive FlexibilityK08NS114170 · NINDS · UNIVERSITY OF WASHINGTON · PI NOLAN, AMBER L · 2019 to 2023
$1.0M
Impact of aging on immune activation and cognitive decline after traumatic brain injuryF32AG054126 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRUKOWSKI, KAREN · 2017 to 2018
$128k
NCATS NIH HHS TL1 TR001871NCI NIH HHS R01 CA246722NIAID NIH HHS P30 AI027763NIA NIH HHS F32 AG054126NIA NIH HHS R01 AG056770NIGMS NIH HHS R25 GM056847NINDS NIH HHS K08 NS114170
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is one of the leading causes of long-term neurological disability in the world. Currently, there are no therapeutics for treating the deleterious consequences of brain trauma; this is in part due to a lack of complete understanding of cellular processes that underlie TBI-related pathologies. Following TBI, microglia, the brain resident immune cells, turn into a "reactive" state characterized by the production of inflammatory mediators that contribute to the development of cognitive deficits. Utilizing multimodal, state-of-the-art techniques that widely span from ultrastructural analysis to optogenetic interrogation of circuit function, we investigated the reactive microglia phenotype one week after injury when learning and memory deficits are also measured. Microglia displayed increased: (i) phagocytic activity in vivo, (ii) synaptic engulfment, (iii) increased neuronal contact, including with dendrites and somata (termed 'satellite microglia'). Functionally, satellite microglia might impact somatic inhibition as demonstrated by the associated reduction in inhibitory synaptic drive. Cumulatively, here we demonstrate novel microglia-mediated mechanisms that may contribute to synaptic loss and cognitive impairment after traumatic brain injury.

Indexed as

Brain Injuries, TraumaticCognitive DysfunctionAnimalsBrainDisease Models, AnimalMiceMice, Inbred C57BLMicrogliaLearning and memoryMicrogliaNeuroinflammationTraumatic brain injury

Identifiers

PMID34403733
PMCPMC9119574
OpenAlexW3195795111

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.