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(Stroke. 2009;40:S119.)
© 2009 American Heart Association, Inc.

Neuroprotection

Potential Molecular Targets for Translational Stroke Research

From the Department of Neurology (P.S.V., J.C.), University of Pittsburgh School of Medicine, Pittsburgh, Pa; and the Geriatric Research, Educational and Clinical Center (J.C.), Veterans Affairs Pittsburgh Health Care System, Pittsburgh, Pa.

Correspondence to Jun Chen, MD, Department of Neurology, S-507, BST, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213. E-mail chenj2@upmc.edu

Key Words: molecular targets • neuroprotection • translational stroke research

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
The stroke research community is currently at a crossroads, and a shift in focus is necessary to propel basic research forward to develop clinically effective therapeutics. In-depth analysis of the past failures and imposing more stringent standards on future basic research experiments will greatly improve the success of translational research. The purpose of this review is to outline proposed revisions in basic research criteria and offer attractive molecular candidates to mitigate brain damage after cerebral ischemia.

A major pitfall encompassing translational stroke research is that a majority of clinical trials conducted have focused on agents involving recanalization of vessels and on excitotoxicity to reduce neuronal death in the penumbra.¹ Recanalization using tissue plasminogen activator only modestly improves patient outcome, and inhibiting excitotoxicity has shown no clinical benefit.² The short duration of excitotoxicity after ischemia does not provide an adequate time window for effective stroke therapy in clinical practice because the exact onset of stroke is often indeterminate and a majority of patients do not seek medical treatment for many hours after the insult. A more reasonable therapeutic window, and hence a greater potential for clinical success, is likely to be attained by placing emphasis on ameliorating the effects of the synergistic processes of programmed cell death (PCD) and inflammation that are active for hours to days after ischemia.³

In addition, it is necessary to identify molecular mediators of ischemic neuroprotection suitable for translation to human clinical trials. Accordingly, more stringent criteria for selection of targets are required. The following criteria . . . [Full Text of this Article]