Susser E, Brown A S, Klonowski E, Allen R H, Lindenbaum J
Department of Psychiatry, Columbia University, New York, New York, USA.
Biol Psychiatry. 1998 Jul 15;44(2):141-3. doi: 10.1016/s0006-3223(97)00427-7.
An increased risk of both schizophrenia and neural tube defects was observed in a birth cohort exposed to famine during early gestation. Neural tube defects have been related to a folate-sensitive genetic defect in homocysteine metabolism. If this were also true for schizophrenia, then cases with low folate (LF)--and only these cases--should have increased homocysteine levels compared with controls.
We compared homocysteine levels of schizophrenia cases and normal controls with low folate (LF) and without low folate (non-LF). Low folate was defined by the bottom tertile for controls.
In the LF group (6 cases, 8 controls), mean homocysteine was 10.7 microM in cases compared with 7.7 microM in controls (p = .03). In the non-LF group (11 cases, 16 controls) mean homocysteine did not differ for cases and controls.
These pilot data are compatible with the hypothesis that a folate-sensitive defect in homocysteine metabolism contributes to cases of schizophrenia.
在孕期早期遭受饥荒的出生队列中,观察到精神分裂症和神经管缺陷的风险均增加。神经管缺陷与同型半胱氨酸代谢中对叶酸敏感的基因缺陷有关。如果精神分裂症也是如此,那么与对照组相比,低叶酸(LF)的病例——且只有这些病例——应具有升高的同型半胱氨酸水平。
我们比较了低叶酸(LF)和非低叶酸(非LF)的精神分裂症病例与正常对照组的同型半胱氨酸水平。低叶酸由对照组的最低三分位数定义。
在LF组(6例病例,8名对照)中,病例的平均同型半胱氨酸为10.7微摩尔/升,而对照组为7.7微摩尔/升(p = 0.03)。在非LF组(11例病例,16名对照)中,病例和对照组的平均同型半胱氨酸无差异。
这些初步数据与以下假设相符,即同型半胱氨酸代谢中对叶酸敏感的缺陷导致了精神分裂症病例。