Notably, we demonstrated that the immunological defects in the peripheral monocytes of AD patients are partially regulated by genetic polymorphisms in alcohol-metabolizing enzymes and that the most acetaldehyde-exposed patients carrying the combination of ALDH2*1/*2 and ADH1B*2 showed the most impaired function of peripheral monocytes regardless the similar amounts of alcohol intake. Here, ADH1B is linked to Alzheimer disease.