In 1980s, 65% of all East Boston residents over the age of 65 were recruited in the study of neuroprotective effects of vitamins C and E. None of the people taking vitamin C or vitamin E developed Alzheimer’s disease when followed up in 4.5 years while among vitamin C non-users, 85% developed the disease. Among vitamin E non-users, 14% developed Alzheimer’s (1)

I was shown that supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase (footnote a) activity at the normal level and serotonin (footnote b) concentration for some extent under the condition to induce experimental dementia in experimental animals (2)

High intake of vitamin E from food (tocopherol), but not from supplements (which usually contain alpha-tocopherol), is shown to reduce incidence of Alzheimer’s disease. The most common alpha-tocopherol alone may not be sufficient in the protective effects (3)

Sources

1. MC Morris et al, Vitamin E and Vitamin C Supplement Use and Risk of Incident Alzheimer Disease. Alzheimer Disease & Associated Disorders, 1998 – V12 – 3
2. LEE Lilha et al., Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia, Journal of nutritional science and vitaminology, 2001, vol. 47, no5, pp. 323-328
3. MC  Morris et. al., Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Am J Clin Nutrition, Vol. 81, No. 2, 508-514, February 2005

Footnotes

a) Acetylcholinesterase (AChE) is an enzyme that degrades  the neurotransmitter acetylcholine at neuromuscular junctions and cholinergic synaptic transmission in the brain.

b) Serotonin is a neurotransmitter found in the central nervous system. It is best known as a “happiness hormone” though it’s no hormone but monoamine.

Combined deficiency in vitamins C and E is a risk factor for neuronal death and brain necrosis.

Vitamin C easily crosses the blood brain barrier and its transport into the brain is mediated by glucose transporters. Vitamin C concentrations in the brain exceed those in blood by 10-fold. In humans, hypovitaminosis C correlated with brain damage in patients with head trauma (Stroke. 2001;32:898-902). The vitamin C has important functions in the brain, for example, protecting neuronal membranes from oxidative damage acting as a scavenger of free radicals.

Another free radical scavenger Vitamin E (-tocopherol) inhibits the amyloid peptide characteristic for Alzheimer’s disease known to induced cell death (Biochemical and Biophysical Research Communications Volume 186, Issue 2, 31 July 1992, Pages 944-950).

The results of a study of Guinea Pigs’s fed either on normal or vitamin-deficient diets showed that while moderate deficiencies of vitamins E or C didn’t result in serious brain changes, their combined moderate deficienciescaused degenerative changes in the guinea pig brains in only 5 days after vitamins were removed from the feed.

Interestingly, the deficiencies in either E or C vitamins had only moderate consequences, but their combination caused severe brain lesions – inflammation, cell death with necrosis and apoptosis and animals’ death (Nutr. 136:1576-1581, June 2006).