Evidence map›Paper›PMID 29898739›Full record

ArticleJournal of neuroinflammation2018

Longitudinal chemokine profile expression in a blood-brain barrier model from Alzheimer transgenic versus wild-type mice.

J Vérité, T Janet, D Chassaing, B Fauconneau, H Rabeony, G Page

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.5field-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

7 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. T Cells Trafficking into the Brain in Aging and Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Review
  4. Review
  5. The intricate role of CCL5/CCR5 axis in Alzheimer disease.Journal of neuropathology and experimental neurology · 2023
    Review
  6. Article
  7. Review
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.

J VéritéEA3808, molecular Targets and Therapeutics of Alzheimer's disease, University of Poitiers, 86073, Poitiers, France.
T JanetEA3808, molecular Targets and Therapeutics of Alzheimer's disease, University of Poitiers, 86073, Poitiers, France.
D ChassaingEA3808, molecular Targets and Therapeutics of Alzheimer's disease, University of Poitiers, 86073, Poitiers, France.
B FauconneauEA3808, molecular Targets and Therapeutics of Alzheimer's disease, University of Poitiers, 86073, Poitiers, France.
H RabeonyEA3808, molecular Targets and Therapeutics of Alzheimer's disease, University of Poitiers, 86073, Poitiers, France.
G PageEA3808, molecular Targets and Therapeutics of Alzheimer's disease, University of Poitiers, 86073, Poitiers, France. guylene.page@univ-poitiers.fr.
Université de Poitiers · FRCentre de Transfert de Technologie du Mans · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease is widely described since the discovery of histopathological lesions in Mrs. Auguste Deter in 1906. However to date, there is no effective treatment to deal with the many cellular and molecular alterations. The complexity is even higher with the growing evidence of involvement of the peripheral blood mononuclear cells (PBMCs). Indeed, monocytes and T cells are shown in the cerebral parenchyma of AD patients, and these cells grafted to the periphery are able to go through the blood-brain barrier (BBB) in transgenic mouse models. It is known that BBB is disrupted at a late stage of AD. Chemokines represent major regulators of the transmigration of PBMCs, but many data were obtained on AD animal models. No data are available on the role of AD BBB in a healthy brain parenchyma. Therefore, the purpose of this study was to analyze the longitudinal chemokine profile expression in a BBB model from AD transgenic mice versus wild-type (WT) mice.

methodsA primary mouse BBB model was used with a luminal compartment either AD or WT and an abluminal compartment WT consisting of astrocytes and microglia. PBMCs were extracted by a ficoll gradient and incubated in the transwell with a direct contact with the luminal side, including the endothelial cells and pericytes. Then, the complete BBB model was incubated during 48 h, before supernatants and cell lysates were collected. Chemokines were quantified by X-MAP® luminex technology.

resultsAbluminal CX3CL1 production increased in 12-month-old AD BBB while CX3CL1 levels decreased in luminal lysates. CCL3 in luminal compartment increased with aging and was significantly different compared to AD BBB at 12 months. In addition, abluminal CCL2 in 12-month-old AD BBB greatly decreased compared to levels in WT BBB. On the contrary, no modification was observed for CCL4, CCL5, and CXCL10.

conclusionThese first findings highlighted the impact of AD luminal compartment on chemokine signature in a healthy brain parenchyma, suggesting new therapeutic or diagnostic approaches.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsATP Binding Cassette Transporter, Subfamily B, Member 1Blood-Brain BarrierCapillary PermeabilityChemokinesDisease Models, AnimalElectric ImpedanceLeukocytes, MononuclearLongitudinal StudiesMaleMiceMice, TransgenicMutationTime FactorsAmyloid beta-Protein PrecursorATP Binding Cassette Transporter, Subfamily B, Member 1ChemokinesAlzheimerBlood-brain barrierChemokinesLongitudinal studyMousePeripheral blood mononuclear cellsPrimary cell culture

Identifiers

PMID29898739
PMCPMC6001165
OpenAlexW2808398392

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.