Research, an association between ex-pression of mitochondrial aldehyde dehydrogenase (ALDH2), a mitochondrial chaperon expressed in the brain, and the prevalence of stroke is revealed. This finding indicates that ALDH2 may serve as a potential endogenous neuroprotective target and a promising therapeutic strategy for the management of stroke.

Stroke is one of the leading causes of death and a major reason of adult chronic disability as well as age-related cognitive decline and dementia [1]. Ischemic stroke represents> 80% of all stroke incidences with the remaining 20% due to primary hemorrhage. Proper management of the conventional risk factors for stroke, such as high blood pressure, elevated blood cholesterol, cigarette smoking, carotid stenosis, diabetes mellitus and heart failure, may reduce the incidence of stroke only to a certain degree, suggesting the existence of undiscovered or undefined risk factors [1, 2]. The unidentified risk factors for stroke, in conjunction with unsatisfactory control of known risk factors (eg, high cholesterol and hypertension), may explain the intimate clinical challenge or failure for stroke management. To this end, identification of novel risk factors may hold promises in the development of strategies for prevention and treatment of stroke. Ample evidence has implicated the importance of genetic predisposition in the onset and progression of stroke [2]. More recently, genome-wide association study (GWAS) approach has transformed the genetics of many complex chronic diseases and is just beginning