Evidence map›Paper›PMID 26170148›Full record

ArticleHistochemistry and cell biology2015

The antimicrobial protein, CAP37, is upregulated in pyramidal neurons during Alzheimer's disease.

Amanda J Brock, Anne Kasus-Jacobi, Megan Lerner, Sreemathi Logan, Adekunle M Adesina, H Anne Pereira

Open access · hybridAbstract read
In one paragraph

Article in Histochemistry and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. NADScience advances · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
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  10. Article
  11. NETosis in Alzheimer's Disease.Frontiers in immunology · 2017
    Review
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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 2 institutions in 1 country.

Amanda J BrockOklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, 1110 N. Stonewall Ave., CPB 255, Oklahoma City, OK, 73117, USA.
Anne Kasus-JacobiOklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, 1110 N. Stonewall Ave., CPB 255, Oklahoma City, OK, 73117, USA.
Megan LernerDepartment of Surgery, University of Oklahoma Health Sciences Center, 1122 NE 13th St., ORB 350, Oklahoma City, OK, 73117, USA.
Sreemathi LoganDepartment of Geriatrics, University of Oklahoma Health Sciences Center, 975 NE 10th St., BRC 1303, Oklahoma City, OK, 73104, USA.
Adekunle M AdesinaDepartment of Pathology, Baylor College of Medicine, One Baylor Plaza, Rm 286A, Houston, TX, 77030, USA.
H Anne PereiraOklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, 1110 N. Stonewall Ave., CPB 255, Oklahoma City, OK, 73117, USA. Anne-Pereira@ouhsc.edu.
University of Oklahoma Health Sciences Center · USBaylor College of Medicine · US

Funding

CAP37 and ocular inflammationR01EY015534 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI PEREIRA, HELOISE ANNE · 2007 to 2011
$1.8M
NEI NIH HHS 5R01EY015534NEI NIH HHS R01 EY015534
6 · The paper itself

Abstract

Inflammation is a well-defined factor in Alzheimer's disease (AD). There is a strong need to identify the molecules contributing to neuroinflammation so that therapies can be designed to prevent immune-mediated neurotoxicity. The cationic antimicrobial protein of 37 kDa (CAP37) is an inflammatory mediator constitutively expressed in neutrophils (PMNs). In addition to antibiotic activity, CAP37 exerts immunomodulatory effects on microglia. We hypothesize that CAP37 mediates the neuroinflammation associated with AD. However, PMNs are not customarily associated with the pathology of AD. This study was therefore designed to identify non-neutrophilic source(s) of CAP37 in brains of AD patients. Brain tissues from patients and age-matched controls were analyzed for CAP37 expression using immunohistochemistry (IHC). To determine factors that induce CAP37 in AD, HCN-1A primary human neurons were treated with tumor necrosis factor-alpha (TNF-α) or amyloid β1-40 (Aβ) and analyzed by IHC. Western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used to confirm CAP37 expression in neurons and brain tissues. IHC revealed CAP37 in cortical neurons in temporal and parietal lobes as well as CA3 and CA4 hippocampal neurons in patients with AD. CAP37 was found in more neurons in AD patients compared with age-matched controls. qRT-PCR and Western blotting showed an increase in CAP37 transcript and protein in the AD temporal lobe, a brain region that is highly impacted in AD. qRT-PCR observations confirmed CAP37 expression in neurons. TNF-α and Aβ increased neuronal expression of CAP37. These findings support our hypothesis that neuronal CAP37 may modulate the neuroinflammatory response in AD.

Indexed as

AdultAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAntimicrobial Cationic PeptidesBlood ProteinsCarrier ProteinsCase-Control StudiesCells, CulturedHumansInflammation MediatorsMaleParietal LobePeptide FragmentsPrimary Cell CultureAmyloid beta-Peptidesamyloid beta-protein (1-40)Antimicrobial Cationic PeptidesAZU1 protein, humanBlood ProteinsCarrier ProteinsInflammation MediatorsPeptide FragmentsTumor Necrosis Factor-alphaAlzheimer’s diseaseAmyloid-betaCAP37MicrogliaNeuroinflammationNeurons

Identifiers

PMID26170148
PMCPMC4575391
OpenAlexW1538811228

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.