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Updated: Mar 18, 2026

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
Published on: October 20, 2016
Vitamin E Status and Neurodegenerative Disease
1a John Tabor Laboratories, Department of Biological and Chemical Sciences , University of Essex , Wivenhoe Park, Colchester , Essex CO4 3SQ , UK.
Abstract:
Vitamin E (alpha-and gamma-tocopherol) may slow the progression of a number of major degenerative diseases of the nervous system that appear to be significantly worsened by oxidative stress. The effects of vitamin E on excitoxicity in cultured neurones is considered, together with ataxia due to vitamin E deficiency (AVED) arising from abetalipoproteinaemia, cholestatic liver disease, cystic fibrosis, short bowel syndrome, total parenteral nutrition, diabetic peripheral neuropathy and familial isolated vitamin E (FIVE) deficiency. Selenium deficiency in Keshan disease is also described in relation to the cardiomyopathy seen in Friedreich's ataxia. Evidence for any beneficial effects of vitamin E upon the course of Friedreich's ataxia, tardive dyskinesia, amyotrophic lateral sclerosis (motor neurone disease), Parkinson's disease, Alzheimer's disease, and Huntington's disease is examined. The application of vitamin E derivatives as protective agents in posttraumatic injury to the nervous system (stroke, head and spinal cord injury and haemorrhage) is discussed.
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