Prolonged central sensory conduction time in alcoholics with hypoactive aldehyde dehydrogenase-2.
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.
Mochizuki
Hitoshi
H
Department of Neurology, National Institute on Alcoholism, Kurihama National Hospital, Yokosuka, Kanagawa, Japan.
Masaki
Toshihiro
T
Yokoyama
Akira
A
Matsushita
Sachio
S
Kamakura
Keiko
K
Motoyoshi
Kazuo
K
Higuchi
Susumu
S
D000079:Acetaldehyde / Q000097:blood / Q000378:metabolism; D000437:Alcoholism / Q000235:genetics* / Q000378:metabolism; D000444:Aldehyde Dehydrogenase / Q000235:genetics*; D000071396:Aldehyde Dehydrogenase, Mitochondrial; D005073:Evoked Potentials, Somatosensory; D006801:Humans; D008297:Male; D008475:Median Nerve / Q000502:physiology; D008875:Middle Aged; D009154:Mutation; D009431:Neural Conduction / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology*
C096127:ALDH2 protein, human; D000444:Aldehyde Dehydrogenase; D000071396:Aldehyde Dehydrogenase, Mitochondrial; D000079:Acetaldehyde