Abstract
People who have a Glu487Lys mutation (single nucleotide polymorphism) in the aldehyde dehydrogenase-2 (ALDH2) gene are slow to metabolize the alcohol breakdown product acetaldehyde. The P13/14-N20 interval of the median nerve somatosensory evoked potential was significantly longer in alcoholic patients with a hypoactive ALDH2 (n = 27) than in those with an active ALDH2 (n = 43). This suggests that acetaldehyde accumulation due to hypoactive ALDH2 is associated with a prolongation of the central sensory conduction time between pons and primary sensory cortex. The present result indicates that an elevated blood concentration of acetaldehyde must cause the central sensory tract involvement and that acetaldehyde is one of factors producing brain damage in alcoholics.
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