Evidence map›Paper›PMID 24309662›Full record

ReviewNature medicine2013

Development, maintenance and disruption of the blood-brain barrier.

Birgit Obermeier, Richard Daneman, Richard M Ransohoff

Abstract readReview
In one paragraph

Review in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,305 papers.

0numbers the graph read from it
0cells of the map it votes in
1,305citing 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

1,305 citing papers in PubMed.

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  20. Simultaneous measurement of water transport across the blood-brain and blood-CSF barrier in the human brain with arterial spin labeling MRI.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Article

1,245 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

3 authors.

Birgit ObermeierNeuroinflammation Research Center, Department of Neuroscience, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.ORCID 000000029248684X
Richard Daneman
Richard M Ransohoff

Funding

Mentored Research: Chemokine Regulation on CNS Inflammation in MSK24NS051400 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI RANSOHOFF, RICHARD M. · 2006 to 2014
$1.4M
Modulating chemokine receptors at the blood-brain barrier under flowR21NS074820 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI RANSOHOFF, RICHARD M. · 2011 to 2012
$432k
NINDS NIH HHS K24 NS051400NINDS NIH HHS R21 NS074820
6 · The paper itself

Abstract

The interface between the blood circulation and the neural tissue features unique characteristics that are encompassed by the term 'blood-brain barrier' (BBB). The main functions of this barrier, namely maintenance of brain homeostasis, regulation of influx and efflux transport, and protection from harm, are determined by its specialized multicellular structure. Every constituent cell type makes an indispensable contribution to the BBB's integrity. But if one member of the BBB fails, and as a result the barrier breaks down, there can be dramatic consequences and neuroinflammation and neurodegeneration can occur. In this Review, we highlight recently gained mechanistic insights into the development and maintenance of the BBB. We then discuss how BBB disruption can cause or contribute to neurological disease. Finally, we examine how this knowledge can be used to explore new possibilities for BBB repair.

Indexed as

AnimalsBlood-Brain BarrierBlood VesselsBrainHumansNeovascularization, PhysiologicNervous System DiseasesVascular Endothelial Growth Factor AWnt Signaling PathwayVascular Endothelial Growth Factor A

Identifiers

PMID24309662
PMCPMC4080800

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.