In:
Annals of Neurology, Wiley, Vol. 35, No. 3 ( 1994-03), p. 298-303
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.
Type of Medium:
Online Resource
ISSN:
0364-5134
,
1531-8249
DOI:
10.1002/ana.410350309
Language:
English
Publisher:
Wiley
Publication Date:
1994
detail.hit.zdb_id:
2037912-2