Dexter D T, Brooks D J, Harding A E, Burn D J, Muller D P, Goss-Sampson M A, Jenner P G, Marsden C D
Biomedical Science Division, King's College, London, UK.
Ann Neurol. 1994 Mar;35(3):298-303. doi: 10.1002/ana.410350309.
Four patients with vitamin E deficiency and sensory ataxia were studied using [18F]dopa positron emission tomography. The 2 most disabled patients, who had severe and prolonged vitamin E deficiency due to abetalipoproteinemia, showed reduced [18F]dopa uptake in both putamen and caudate. Putaminal uptake was in a similar range to that seen in Parkinson's disease. Studies of [3H]mazindol binding in the striatum of vitamin E--deficient rats indicated a reduced number of dopamine terminals, which was most severe in ventrolateral striatum. These observations suggest that severe and prolonged vitamin E deficiency results in loss of nigrostriatal nerve terminals, and support the hypothesis that oxidative stress may contribute to the etiology of Parkinson's disease.
对4例维生素E缺乏伴感觉性共济失调的患者进行了[18F]多巴正电子发射断层扫描研究。2例残疾最严重的患者因无β脂蛋白血症而存在严重且长期的维生素E缺乏，其壳核和尾状核的[18F]多巴摄取均减少。壳核摄取与帕金森病患者所见范围相似。对维生素E缺乏大鼠纹状体中[3H]吗吲哚结合的研究表明多巴胺终末数量减少，在腹外侧纹状体最为严重。这些观察结果提示，严重且长期的维生素E缺乏会导致黑质纹状体神经终末丧失，并支持氧化应激可能促成帕金森病病因学的假说。
