Breaking down brain barrier breaches in cerebral malaria

Research output: Contribution to journal › Comment/debate › Research › peer-review

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Breaking down brain barrier breaches in cerebral malaria. / Petersen, Jens E V; Lavstsen, Thomas; Craig, Alister.

In: Journal of Clinical Investigation, Vol. 126, No. 10, 03.10.2016, p. 3725-3727.

Research output: Contribution to journal › Comment/debate › Research › peer-review

Harvard

Petersen, JEV, Lavstsen, T & Craig, A 2016, 'Breaking down brain barrier breaches in cerebral malaria', Journal of Clinical Investigation, vol. 126, no. 10, pp. 3725-3727. https://doi.org/10.1172/JCI90188

APA

Petersen, J. E. V., Lavstsen, T., & Craig, A. (2016). Breaking down brain barrier breaches in cerebral malaria. Journal of Clinical Investigation, 126(10), 3725-3727. https://doi.org/10.1172/JCI90188

Vancouver

Petersen JEV, Lavstsen T, Craig A. Breaking down brain barrier breaches in cerebral malaria. Journal of Clinical Investigation. 2016 Oct 3;126(10):3725-3727. https://doi.org/10.1172/JCI90188

Author

Petersen, Jens E V ; Lavstsen, Thomas ; Craig, Alister. / Breaking down brain barrier breaches in cerebral malaria. In: Journal of Clinical Investigation. 2016 ; Vol. 126, No. 10. pp. 3725-3727.

Bibtex

@article{cd5270a1d23c4a48a2171f761a1f173f,
title = "Breaking down brain barrier breaches in cerebral malaria",
abstract = "Recent findings have linked brain swelling to death in cerebral malaria (CM). These observations have prompted a number of investigations into the mechanisms of this pathology with the goal of identifying potential therapeutic targets. In this issue of the JCI, Gallego-Delgado and colleagues present evidence that implicates angiotensin receptors and the relocation of β-catenin to the endothelial cell nucleus in CM. This study provides a renewed focus on infected erythrocyte debris as the cause of endothelial damage and challenges previous work implicating direct effects of infected erythrocyte sequestration in the brain as the major driver of disease. While this work provides potential therapeutic avenues for CM, it leaves a number of questions unanswered.",
author = "Petersen, {Jens E V} and Thomas Lavstsen and Alister Craig",
year = "2016",
month = oct,
day = "3",
doi = "10.1172/JCI90188",
language = "English",
volume = "126",
pages = "3725--3727",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "American Society for Clinical Investigation",
number = "10",

}

RIS

TY - JOUR

T1 - Breaking down brain barrier breaches in cerebral malaria

AU - Petersen, Jens E V

AU - Lavstsen, Thomas

AU - Craig, Alister

PY - 2016/10/3

Y1 - 2016/10/3

N2 - Recent findings have linked brain swelling to death in cerebral malaria (CM). These observations have prompted a number of investigations into the mechanisms of this pathology with the goal of identifying potential therapeutic targets. In this issue of the JCI, Gallego-Delgado and colleagues present evidence that implicates angiotensin receptors and the relocation of β-catenin to the endothelial cell nucleus in CM. This study provides a renewed focus on infected erythrocyte debris as the cause of endothelial damage and challenges previous work implicating direct effects of infected erythrocyte sequestration in the brain as the major driver of disease. While this work provides potential therapeutic avenues for CM, it leaves a number of questions unanswered.

AB - Recent findings have linked brain swelling to death in cerebral malaria (CM). These observations have prompted a number of investigations into the mechanisms of this pathology with the goal of identifying potential therapeutic targets. In this issue of the JCI, Gallego-Delgado and colleagues present evidence that implicates angiotensin receptors and the relocation of β-catenin to the endothelial cell nucleus in CM. This study provides a renewed focus on infected erythrocyte debris as the cause of endothelial damage and challenges previous work implicating direct effects of infected erythrocyte sequestration in the brain as the major driver of disease. While this work provides potential therapeutic avenues for CM, it leaves a number of questions unanswered.

U2 - 10.1172/JCI90188

DO - 10.1172/JCI90188

M3 - Comment/debate

C2 - 27643435

VL - 126

SP - 3725

EP - 3727

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 10

ER -

ID: 167362381