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Stroke. 2009;40:S4-S7
Published online before print December 8, 2008, doi: 10.1161/STROKEAHA.108.534388
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(Stroke. 2009;40:S4.)
© 2009 American Heart Association, Inc.


Neurovascular Unit

Dysfunctional Cell-Cell Signaling in the Neurovascular Unit as a Paradigm for Central Nervous System Disease

Shuzhen Guo, PhD Eng H. Lo, PhD

From the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Program in Neuroscience, Harvard Medical School, Charlestown, Mass.

Correspondence to Eng H. Lo, PhD, Neuroprotection Research Laboratory, MGH East 149-2401, 13th Street, Charlestown, MA 02129. E-mail Lo{at}helix.mgh.harvard.edu

The fundamental premise of neuroprotection has historically focused on the prevention of neuronal death. However, despite tremendous advances in the molecular biology of intraneuronal mechanisms and pathways, a clinically effective neuroprotectant does not yet exist. This problem is especially clear for stroke, for which a large number of neuroprotection trials have failed. The concept of the neurovascular unit emphasizes that cell-cell signaling among the various neuronal, glial, and vascular compartments underlies the homeostasis of normal brain function. Conversely, dysfunctional signaling within the neurovascular unit should contribute to disease. This minireview surveys recent data that support this basic idea, with examples drawn from experimental models broadly relevant to stroke and neurodegeneration.


Key Words: neuroprotection • cell-cell signaling




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