Evidence map›Paper›PMID 23108061›Full record

ArticleBrain, behavior, and immunity2013

PPARγ activation prevents impairments in spatial memory and neurogenesis following transient illness.

Brandi K Ormerod, Simon J Hanft, Aditya Asokan, Ursula Haditsch, Star W Lee, Theo D Palmer

Abstract read
In one paragraph

Article in Brain, behavior, and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

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  9. The role of sleep disturbance and inflammation for spatial memory.Brain, behavior, & immunity - health · 2021
    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.

Brandi K OrmerodInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA 94305, USA; J. Crayton Pruitt Family Department of Biomedical Engineering, McKnight Brain Institute and Neuroscience Department, University of Florida, Gainesville, FL 32611, USA. Electronic address: bormerod@bme.ufl.edu.
Simon J HanftInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA 94305, USA.
Aditya AsokanJ. Crayton Pruitt Family Department of Biomedical Engineering, McKnight Brain Institute and Neuroscience Department, University of Florida, Gainesville, FL 32611, USA.
Ursula HaditschInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA 94305, USA.
Star W LeeInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA 94305, USA.
Theo D PalmerInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University, Stanford, CA 94305, USA. Electronic address: tpalmer@stanford.edu.

Funding

Integrin/ECM gating of adult neural stem cell activityR01MH085911 · NIMH · STANFORD UNIVERSITY · PI PALMER, THEO D · 2010 to 2014
$2.0M
Neural Stem Cell Dysfunction in Delayed Radiation InjuryR01NS045113 · NINDS · STANFORD UNIVERSITY · PI PALMER, THEO D · 2003 to 2006
$1.5M
Inflammatory Modulation of Neural Stem Cell FunctionR01MH071472 · NIMH · STANFORD UNIVERSITY · PI PALMER, THEO D · 2005 to 2009
$1.5M
Preserving Neurogenesis and Cognition with NSAID'SR21NS050549 · NINDS · STANFORD UNIVERSITY · PI PALMER, THEO D · 2005 to 2006
$360k
NIMH NIH HHS R01 MH071472NIMH NIH HHS R01 MH085911NINDS NIH HHS R01 NS045113NINDS NIH HHS R21 NS050549
6 · The paper itself

Abstract

The detrimental effects of illness on cognition are familiar to virtually everyone. Some effects resolve quickly while others may linger after the illness resolves. We found that a transient immune response stimulated by lipopolysaccharide (LPS) compromised hippocampal neurogenesis and impaired hippocampus-dependent spatial memory. The immune event caused an ∼50% reduction in the number of neurons generated during the illness and the onset of the memory impairment was delayed and coincided with the time when neurons generated during the illness would have become functional within the hippocampus. Broad spectrum non-steroidal anti-inflammatory drugs attenuated these effects but selective Cox-2 inhibition was ineffective while PPARγ activation was surprisingly effective at protecting both neurogenesis and memory from the effects of LPS-produced transient illness. These data may highlight novel mechanisms behind chronic inflammatory and neuroinflammatory episodes that are known to compromise hippocampus-dependent forms of learning and memory.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalAntimetabolitesBromodeoxyuridineCell CountData Interpretation, StatisticalFemaleHippocampusIllness BehaviorImmunohistochemistryLearningLipopolysaccharidesMaze LearningMemoryMiceMice, Inbred C57BLAnti-Inflammatory Agents, Non-SteroidalAntimetabolitesBromodeoxyuridineLipopolysaccharidesPPAR gamma

Identifiers

PMID23108061
PMCPMC3570721

What OpenQuestion holds

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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.