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Nigrostriatal function in vitamin E deficiency: Clinical, experimental, and positron emission tomographic studies

✍ Scribed by David T. Dexter; David J. Brooks; Prof A. E. Harding; David J. Burn; David P. R. Muller; M. A. Goss-Sampson; P. G. Jenner; C. David Marsden

Publisher: John Wiley and Sons
Year: 1994
Tongue: English
Weight: 602 KB
Volume: 35
Category: Article
ISSN: 0364-5134
DOI: 10.1002/ana.410350309

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✦ Synopsis

Abstract

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.

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