Dexter, D. T., Brooks, D. J., Harding, A. E., Burn, D. J., Muller, D. P., Goss-Sampson, M. A. ORCID: 0000-0002-2662-559X, Jenner, P. G. and Marsden, C. D. (1994) Nigrostriatal function in vitamin E deficiency: clinical, experimental, and positron emission tomographic studies. Annals of neurology, 35 (3). pp. 298-303. ISSN 0364-5134 (Print), 1531-8249 (Online) (doi:https://doi.org/10.1002/ana.410350309)

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Abstract

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.

Item Type:	Article
Uncontrolled Keywords:	Vitamin E
Faculty / School / Research Centre / Research Group:	Faculty of Engineering & Science Faculty of Education, Health & Human Sciences > School of Human Sciences (HUM)
Last Modified:	09 Oct 2021 04:46
URI:	http://gala.gre.ac.uk/id/eprint/12384

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