Evidence map›Paper›PMID 9713826›Full record

ArticleMolecular medicine (Cambridge, Mass.)1998

Amyloid-beta induces chemokine secretion and monocyte migration across a human blood--brain barrier model.

M Fiala, L Zhang, X Gan, B Sherry, D Taub, M C Graves, S Hama, D Way, M Weinand, M Witte and 3 more

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

Article in Molecular medicine (Cambridge, Mass.), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

93 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025
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33 more citing papers are in PubMed but not listed here.

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

13 authors at 5 institutions in 1 country.

M FialaDepartment of Medicine, UCLA School of Medicine, Los Angeles, California, USA. fiala@ucla.edu
L Zhang
X Gan
B Sherry
D Taub
M C Graves
S Hama
D Way
M Weinand
M Witte
D Lorton
Y M Kuo
A E Roher
University of California, Los Angeles · USBanner Sun Health Research Institute · USUniversity of Arizona · USNational Institute on Aging · USUCLA Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAside from numerous parenchymal and vascular deposits of amyloid beta (A beta) peptide, neurofibrillary tangles, and neuronal and synaptic loss, the neuropathology of Alzheimer's disease is accompanied by a subtle and chronic inflammatory reaction that manifests itself as microglial activation. However, in Alzheimer's disease, alterations in the permeability of the blood-brain barrier and chemotaxis, in part mediated by chemokines and cytokines, may permit the recruitment and transendothelial passage of peripheral cells into the brain parenchyma. MATERIALS AND

methodsHuman monocytes from different donors were tested for their capacity to differentiate into macrophages and their ability to secrete cytokines and chemokines in the presence of A beta 1-42. A paradigm of the blood-brain barrier was constructed utilizing human brain endothelial and astroglial cells with the anatomical and physiological characteristics observed in vivo. This model was used to test the ability of monocytes/macrophages to transmigrate when challenged by A beta 1-42 on the brain side of the blood-brain barrier model.

resultsIn cultures of peripheral monocytes, A beta 1-42 induced the secretion of proinflammatory cytokines TNF-alpha, IL-6, IL-1 beta, and IL-12, as well as CC chemokines MCP-1, MIP-1 alpha, and MIP-1 beta, and CXC chemokine IL-8 in a dose-related fashion. In the blood-brain barrier model, A beta 1-42 and monocytes on the brain side potentiated monocyte transmigration from the blood side to the brain side. A beta 1-42 stimulated differentiation of monocytes into adherent macrophages in a dose-related fashion. The magnitude of these proinflammatory effects of A beta 1-42 varied dramatically with monocytes from different donors.

conclusionIn some individuals, circulating monocytes/macrophages, when recruited by chemokines produced by activated microglia and macrophages, could add to the inflammatory destruction of the brain in Alzheimer's disease.

Indexed as

Blood-Brain BarrierCell MovementAlzheimer DiseaseAmyloid beta-PeptidesAstrocytesCell DifferentiationCells, CulturedChemokinesDose-Response Relationship, DrugEndothelium, VascularHumansInflammationInterleukinsMacrophagesModels, BiologicalMonocytesAmyloid beta-Peptidesamyloid beta-protein (1-42)ChemokinesInterleukinsPeptide FragmentsTumor Necrosis Factor-alpha

Identifiers

PMID9713826
PMCPMC2230332
OpenAlexW2221521015

What OpenQuestion holds

Textmetadata
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.