Nature Search

Disruption of astrocyte–vascular coupling and the blood–brain barrier by invading glioma cells

Astrocytic endfeet maintain endothelial tight junctions that form the blood–brain barrier (BBB), which can be damaged by invading gliomas. Here, the authors show that this damage is due to the association of gliomas with existing vessels and the displacement of astrocytic endfeet.

Stacey Watkins
Stefanie Robel
Harald Sontheimer
Research19 Jun 2014
Nature Communications

Volume: 5, P: 1-15
Optimized enrichment of murine blood–brain barrier vessels with a critical focus on network hierarchy in post-collection analysis

Hanaa Abdelazim
Audra Barnes
John C. Chappell
ResearchOpen Access06 May 2025
Scientific Reports

Volume: 15, P: 1-15
Glutamate release by primary brain tumors induces epileptic activity

People with brain cancers called gliomas often have seizures due to secretion of the excitatory neurotransmitter glutamate from the tumor. Now, Harald Sontheimer and his colleagues report that blockade of a cystine-glutamate transporter in tumor cells by an FDA-approved drug can reduce glioma-induced epilepsy in mice.

Susan C Buckingham
Susan L Campbell
Harald Sontheimer
Research11 Sept 2011
Nature Medicine

Volume: 17, P: 1269-1274
A neurocentric perspective on glioma invasion

Malignant gliomas are notoriously difficult cancers to treat. The majority of current therapeutics target the traditional oncological traits of glioma cells. In this Review, Cuddapahet al. explore the unique biology of glioma cells and propose novel, brain-specific therapeutic targets.

Vishnu Anand Cuddapah
Stefanie Robel
Harald Sontheimer
Reviews20 Jun 2014
Nature Reviews Neuroscience

Volume: 15, P: 455-465
The stem cell potential of glia: lessons from reactive gliosis

In the adult brain, neurogenesis occurs in a few restricted niches. However, the activation of glia following brain injury can endow these cells with stem cell properties. Götz and colleagues discuss how a more detailed knowledge of reactive gliosis might enable the stem cell potential of glia to be harnessed.

Stefanie Robel
Benedikt Berninger
Magdalena Götz
Reviews20 Jan 2011
Nature Reviews Neuroscience

Volume: 12, P: 88-104
Reactive astrocyte nomenclature, definitions, and future directions

Good–bad binary classifications fail to describe reactive astrocytes in CNS disorders. Here, 81 researchers reach consensus on widespread misconceptions and provide definitions and recommendations for future research on reactive astrocytes.

Carole Escartin
Elena Galea
Alexei Verkhratsky
Reviews15 Feb 2021
Nature Neuroscience

Volume: 24, P: 312-325
Glia as drivers of abnormal neuronal activity

Reactive astrocytes have been proposed to become incompetent bystanders in epilepsy as a result of cellular changes rendering them incapable of performing housekeeping tasks. This review discusses new research that suggests that reactive astrocytes may drive the disease process by impairing the inhibitory action of neuronal GABA receptors.

Stefanie Robel
Harald Sontheimer
Reviews29 Dec 2015
Nature Neuroscience

Volume: 19, P: 28-33
Multi-omics signatures of alcohol use disorder in the dorsal and ventral striatum

Lea Zillich
Eric Poisel
Stephanie H. Witt
ResearchOpen Access06 May 2022
Translational Psychiatry

Volume: 12, P: 1-9
Epigenome-wide association study of alcohol use disorder in five brain regions

Lea Zillich
Josef Frank
Stephanie H. Witt
ResearchOpen Access13 Nov 2021
Neuropsychopharmacology

Volume: 47, P: 832-839
Serotonin Depletion Hampers Survival and Proliferation in Neurospheres Derived from Adult Neural Stem Cells

Jens Benninghoff
Angela Gritti
Angelo Luigi Vescovi
Research09 Dec 2009
Neuropsychopharmacology

Volume: 35, P: 893-903
Oxytocin Reduces Alcohol Cue-Reactivity in Alcohol-Dependent Rats and Humans

Anita C Hansson
Anne Koopmann
Rainer Spanagel
Research01 Nov 2017
Neuropsychopharmacology

Volume: 43, P: 1235-1246
Differential Roles for L-Type Calcium Channel Subtypes in Alcohol Dependence

Stefanie Uhrig
David Vandael
Anita C Hansson
Research01 Dec 2016
Neuropsychopharmacology

Volume: 42, P: 1058-1069

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