Evidence map›Paper›PMID 24315728›Full record

ArticleNeurobiology of aging2014

Age and duration of inflammatory environment differentially affect the neuroimmune response and catecholaminergic neurons in the midbrain and brainstem.

Isabelle Bardou, Roxanne M Kaercher, Holly M Brothers, Sarah C Hopp, Sarah Royer, Gary L Wenk

Abstract read
In one paragraph

Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 13% 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

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

  1. Pooled it
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  3. Article
  4. Review
  5. Article
  6. Role of cytokines and reactive oxygen species in brain aging.Mechanisms of ageing and development · 2023
    Review
  7. Article
  8. Effects ofArchives of Razi Institute · 2022
    Article
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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

6 authors at 1 institution in 1 country.

Isabelle BardouDepartment of Psychology, The Ohio State University, Columbus, OH, USA; Department of Neuroscience, The Ohio State University, Columbus, OH, USA.
Roxanne M KaercherDepartment of Psychology, The Ohio State University, Columbus, OH, USA; Department of Neuroscience, The Ohio State University, Columbus, OH, USA.
Holly M BrothersDepartment of Psychology, The Ohio State University, Columbus, OH, USA; Department of Neuroscience, The Ohio State University, Columbus, OH, USA.
Sarah C HoppDepartment of Psychology, The Ohio State University, Columbus, OH, USA; Department of Neuroscience, The Ohio State University, Columbus, OH, USA.
Sarah RoyerDepartment of Psychology, The Ohio State University, Columbus, OH, USA; Department of Neuroscience, The Ohio State University, Columbus, OH, USA.
Gary L WenkDepartment of Psychology, The Ohio State University, Columbus, OH, USA; Department of Neuroscience, The Ohio State University, Columbus, OH, USA. Electronic address: wenk.6@osu.edu.
The Ohio State University · US

Funding

Vulnerability to neuroinflammation of brainstem ascending aminergic systemsR01AG037320 · NIA · OHIO STATE UNIVERSITY · PI WENK, GARY L. · 2011 to 2015
$1.5M
Aging microglia-neuronal communicationR01AG030331 · NIA · OHIO STATE UNIVERSITY · PI WENK, GARY L. · 2008 to 2012
$1.3M
NIA NIH HHS R01 AG030331NIA NIH HHS R01 AG037320
6 · The paper itself

Abstract

Neuroinflammation and degeneration of ascending catecholaminergic systems occur early in the neurodegenerative process. Age and the duration of a pro-inflammatory environment induced by continuous intraventricular lipopolysaccharide (LPS) differentially affect the expression profile of pro- and anti-inflammatory genes and proteins as well as the number of activated microglia (express major histocompatibility complex II; MHC II) and the integrity and density of ascending catecholaminergic neural systems originating from the locus coeruleus (LC) and substantia nigra pars compacta (SNpc) in rats. LPS infusion increased gene expression and/or protein levels for both pro- and anti-inflammatory biomarkers. Although LPS infusion stimulated a robust increase in IL-1ß gene and protein expression, this increase was blunted with age. LPS infusion also increased the density of activated microglia cells throughout the midbrain and brainstem. Corresponding to the development of a pro-inflammatory environment, LC and SNpc neurons immunopositive for tyrosine-hydroxylase (the rate-limiting synthetic enzyme for dopamine and norepinephrine) decreased in number, along with a decrease in tyrosine-hydroxylase gene expression in the midbrain and/or brainstem region. Our data support the concept that continuous exposure to a pro-inflammatory environment drives exaggerated changes in the production and release of inflammatory mediators that interact with age to impair functional capacity of the SNpc and LC.

Indexed as

AgingAnimalsCatecholaminesGene ExpressionInflammationInflammation MediatorsInterleukin-1betaLipopolysaccharidesLocus CoeruleusMaleMicrogliaNeurodegenerative DiseasesNeuroimmunomodulationNeuronsPeptide FragmentsRatsCatecholaminesInflammation MediatorsInterleukin-1betainterleukin-1beta (163-171)LipopolysaccharidesPeptide FragmentsTyrosine 3-MonooxygenaseAgingAlzheimer's diseaseCytokinesLocus coeruleusMicrogliaNeuroinflammationParkinson's diseaseRatSubstantia nigra

Identifiers

PMID24315728
PMCPMC3946275
OpenAlexW2143539224

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.