Translational Strategies for Neuroprotection in Ischemic Stroke—Focusing on Acid-Sensing Ion Channel 1a

Jan 7, 2014Translational stroke research

Approaches to protect the brain from stroke focusing on acid-sensing ion channel 1a

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Abstract

Acid-sensing ion channels (ASICs) may contribute to poor stroke prognosis due to localized drops in brain pH.

Ischemic stroke is a leading cause of death and long-term disability.
Existing treatment options for stroke are limited and time-sensitive.
Glutamate receptor antagonists have not been successful in clinical trials.
Excessive calcium overload from glutamate receptor activation initiates injury in stroke.
Research on ASICs suggests they could play a significant role in stroke-related damage.

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Ischemic stroke contributes to the majority of brain injuries and remains to be a leading cause of death and long-term disability. Despite the devastating pathology and high incidence of disease, there remain only few treatment options (TPA and endovascular procedures), which may be hampered by time-dependent administration among a variety of other factors. Promising research of glutamate receptor antagonists has been unsuccessful in clinical trial. But, the mechanism by which glutamate receptors initiate injury by excessive calcium overload has spurred investigation of new and potentially successful candidates for stroke therapy. Acid-sensing ion channels (ASICs) may contribute to poor stroke prognosis due to localized drop in brain pH, resulting in excessive calcium overload, independent of glutamate activation. Accumulating studies targeting ASICs have underscored the importance of understanding inhibition, regulation, desensitization, and trafficking of this channel and its role in disease. This review will discuss potential directions in translational ASIC research for future stroke therapies.

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Abstract

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