Evidence map›Paper›PMID 24607962›Full record

ArticleJournal of neuropathology and experimental neurology2014

Age-related brain expression and regulation of the chemokine CCL4/MIP-1β in APP/PS1 double-transgenic mice.

Min Zhu, Joanne S Allard, Yongqing Zhang, Evelyn Perez, Edward L Spangler, Kevin G Becker, Peter R Rapp

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

34 citing papers in PubMed, 67 citations in OpenAlex.

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  12. Neutrophil-Mediated Progression of Mild Cognitive Impairment to Dementia.International journal of molecular sciences · 2023
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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

7 authors at 4 institutions in 1 country.

Min ZhuFrom the Neurocognitive Aging Section (MZ, EP, ELS, PRR), and Gene Expression and Genomics Unit (YZ, KGB), National Institutes of Health, National Institute on Aging, Intramural Research Program, Biomedical Research Center, Baltimore, Maryland; and Department of Physiology and Biophysics, Howard University College of Medicine, Washington, DC (JSA).
Joanne S Allard
Yongqing Zhang
Evelyn Perez
Edward L Spangler
Kevin G Becker
Peter R Rapp
National Institutes of Health · USInstitute on Aging · USHoward University · USNational Institute on Aging · US

Funding

Neurocognitive Aging: Experience-Dependent Dynamics, Plasticity and Network ContributionsZIAAG000350 · NIA · NATIONAL INSTITUTE ON AGING · PI RAPP, PETER R · 2009 to 2025
$30.9M
Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
Intramural NIH HHS Z99 AG999999
6 · The paper itself

Abstract

The detrimental effect of activation of the chemokine CCL4/MIP-1β on neuronal integrity in patients with HIV-associated dementia has directed attention to the potential role of CCL4 expression and regulation in Alzheimer disease. Here, we show that CCL4 mRNA and protein are overexpressed in the brains of APPswe/PS1ΔE9 (APP/PS1) double-transgenic mice, a model of cerebral amyloid deposition; expression was minimal in brains from nontransgenic littermates or single-mutant controls. Increased levels of CCL4 mRNA and protein directly correlated with the age-related progression of cerebral amyloid-β (Aβ) levels in APP/PS1 mice. We also found significantly increased expression of activating transcription factor 3 (ATF3), which was positively correlated with age-related Aβ deposition and CCL4 in the brains of APP/PS1 mice. Results from chromatin immunoprecipitation-quantitative polymerase chain reaction confirmed that ATF3 binds to the promoter region of the CCL4 gene, consistent with a potential role in regulating CCL4 transcription. Finally, elevated ATF3 mRNA expression in APP/PS1 brains was associated with hypomethylation of the ATF3 gene promoter region. These observations prompt the testable hypothesis for future study that CCL4 overexpression, regulated in part by hypomethylation of the ATF3 gene, may contribute to neuropathologic progression associated with amyloid deposition in Alzheimer disease.

Indexed as

Activating Transcription Factor 3AgingAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainChemokine CCL4Chromatin ImmunoprecipitationDisease Models, AnimalEnzyme-Linked Immunosorbent AssayGene Expression RegulationGlial Fibrillary Acidic ProteinMiceMice, Inbred C57BLMice, TransgenicActivating Transcription Factor 3Amyloid beta-PeptidesAmyloid beta-Protein PrecursorAtf3 protein, mouseChemokine CCL4Glial Fibrillary Acidic ProteinPresenilin-1

Identifiers

PMID24607962
PMCPMC3977177
OpenAlexW2333745858

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.