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on December 8, 2008

Stroke. 2008
Published online before print December 8, 2008, doi: 10.1161/STROKEAHA.108.534388
A more recent version of this article appeared on March 1, 2009
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Submitted on August 11, 2008
Accepted on August 12, 2008

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

Shuzhen Guo PhD and 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.

* To whom correspondence should be addressed. E-mail: Lo{at}helix.mgh.harvard.edu.

Abstract—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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