Hulyalkar A R, Nora R, Manowitz P
Alcohol Clin Exp Res. 1984 May-Jun;8(3):337-41. doi: 10.1111/j.1530-0277.1984.tb05524.x.
Leukocytes from 200 mentally ill patients and 100 normal controls were analyzed for electrophoretic variants of arylsulfatase A. Four different variant forms were found in 15 subjects. There is a relatively high occurrence of the arylsulfatase A variants in patients with alcoholism. Twenty-one per cent (12/56) of patients with alcoholism have a variant enzyme. Only one of the 100 normal controls has a variant enzyme. (This single subject was considered normal by the criteria of the study, namely, a self-report of no current medical problem or psychiatric history. However, upon further testing, it was found that this subject has neurological and neuropsychological deficits). The hypothesis is presented that chronic alcohol intake and abnormal arylsulfatase A act in concert to elevate sulfatide levels which results in abnormalities of brain function. If this hypothesis is correct, persons in whom abnormal arylsulfatase A is expressed may be at risk to the neuropathological effects of alcohol.
对200名精神病患者和100名正常对照者的白细胞进行了芳基硫酸酯酶A电泳变异体分析。在15名受试者中发现了四种不同的变异形式。酗酒患者中芳基硫酸酯酶A变异体的发生率相对较高。21%（12/56）的酗酒患者有一种变异酶。100名正常对照者中只有一人有一种变异酶。（根据该研究的标准，这个单一受试者被认为是正常的，即自我报告目前没有医疗问题或精神病史。然而，经过进一步测试，发现这个受试者有神经和神经心理缺陷）。提出的假设是，长期摄入酒精和异常的芳基硫酸酯酶A共同作用，提高硫脂水平，从而导致脑功能异常。如果这个假设正确，表达异常芳基硫酸酯酶A的人可能面临酒精对神经病理作用的风险。
