Evidence map›Paper›PMID 21822589›Full record

ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2012

A lifespan approach to neuroinflammatory and cognitive disorders: a critical role for glia.

Staci D Bilbo, Susan H Smith, Jaclyn M Schwarz

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
7.0field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 127 citations in OpenAlex.

  1. Article
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  4. Review
  5. Review
  6. Article
  7. Article
  8. Hyperammonemia-Associated Delirium Mimics Dementia: A Case Report.Psychiatry and clinical psychopharmacology · 2022
    Article
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  10. Article
  11. Review
  12. Article
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  16. Review
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  19. Placental Macrophages: A Window Into Fetal Microglial Function in Maternal Obesity.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2019
    Article
  20. Article

7 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

3 authors at 1 institution in 1 country.

Staci D BilboDepartment of Psychology & Neuroscience, Duke University, Durham, NC 27708, USA. staci.bilbo@duke.edu
Susan H Smith
Jaclyn M Schwarz
Duke University · US

Funding

Early Life Origins of Risk & Resilience to Drugs of Abuse: Role of Glial PrimingR01DA025978 · NIDA · DUKE UNIVERSITY · PI BILBO, STACI D · 2008 to 2011
$1.0M
Early Life Infection, Neuroinflammation, and MemoryR01MH083698 · NIMH · DUKE UNIVERSITY · PI BILBO, STACI D · 2009 to 2010
$889k
NIDA NIH HHS R01 DA025978NIMH NIH HHS R01 MH083698
6 · The paper itself

Abstract

Cognitive decline is a common problem of aging. Whereas multiple neural and glial mechanisms may account for these declines, microglial sensitization and/or dystrophy has emerged as a leading culprit in brain aging and dysfunction. However, glial activation is consistently observed in normal brain aging as well, independent of frank neuroinflammation or functional impairment. Such variability suggests the existence of additional vulnerability factors that can impact neuronal-glial interactions and thus overall brain and cognitive health. The goal of this review is to elucidate our working hypothesis that an individual's risk or resilience to neuroinflammatory disorders and poor cognitive aging may critically depend on their early life experience, which can change immune reactivity within the brain for the remainder of the lifespan. For instance, early-life infection in rats can profoundly disrupt memory function in young adulthood, as well as accelerate age-related cognitive decline, both of which are linked to enduring changes in glial function that occur in response to the initial infection. We discuss these findings within the context of the growing literature on the role of immune molecules and neuroimmune crosstalk in normal brain development. We highlight the intrinsic factors (e.g., chemokines, hormones) that regulate microglial development and their colonization of the embryonic and postnatal brain, and the capacity for disruption or "re-programming" of this crucial process by external events (e.g., stress, infection). An impact on glia, which in turn alters neural development, has the capacity to profoundly impact cognitive and mental health function at all stages of life.

Indexed as

AgingAnimalsBacterial InfectionsBrainCognition DisordersHumansInflammationNeurogliaNeuroimmunomodulation

Identifiers

PMID21822589
PMCPMC3267003
OpenAlexW2092281141

What OpenQuestion holds

Textmetadata
LicenceTDM
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.