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Nigrostriatal function in vitamin E deficiency: Clinical, experimental, and positron emission tomographic studies
Author(s) -
Dexter David T.,
Brooks David J.,
Harding A. E.,
Burn David J.,
Muller David P. R.,
GossSampson M. A.,
Jenner P. G.,
Marsden C. David
Publication year - 1994
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410350309
Subject(s) - putamen , striatum , positron emission tomography , parkinson's disease , medicine , endocrinology , dopamine , vitamin e deficiency , caudate nucleus , neuroscience , psychology , vitamin e , disease , chemistry , nuclear medicine , biochemistry , antioxidant
Four patients with vitamin E deficiency and sensory ataxia were studied using [ 18 F]dopa positron emission tomography. The 2 most disabled patients, who had severe and prolonged vitamin E deficiency due to abetalipoproteinemia, showed reduced [ 18 F]dopa uptake in both putamen and caudate. Putaminal uptake was in a similar range to that seen in Parkinson's disease. Studies of [ 3 H]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.