Progress and Prospects in Parkinson's Research/Therapy/Neuroprotection/Vitamin E

Background
Vitamin_E is a collection of 8 fat soluble compounds found in sunflower oil and a variety of vegetables including broccoli and avocados. The recommended adult intake is 15mg. per day. It stops the production of reactive oxygen species formed when fat undergoes oxidation.

Research
1987

Perry et al administered massive doses of alpha tocopherol (vitamin E extract) and beta-carotene (precursor to vitamin A) to marmosets with MPTP-induced PD. This did not have any demionstrable effect on their condition.

1990

Odunze et al induced Parkinsonism in mice by the administration of MPTP and then measured levels of Vitamin E. Vitamin E levels in all areas of the brain rose but returned to normal within a few hours except for the substantia nigra. It was conclude that Vitamin E deficient mice were much more susceptible to MPTP toxicity than controls.

1991

Gong et al were fed Vitamin E for 12 weeks prior to being induced with PD by MPTP injections. Their findings were:-

"Mice with elevated cerebral VE were not protected from MPTP toxicity, with DA content as an indicator. In conclusion, these findings indicate that moderate elevation of brain VE is not adequate for protecting DA-containing neurons against the toxic actions of a high dose of MPTP"

1992

Fahn,S. administered high doses of vitamins C and E to a group of PD patients receiving concomitant amantadine and anticholinergics (but not levadopa).

"The time when levodopa became necessary in the treated patients was compared to another group of patients followed elsewhere who did not receive antioxidants. The time when levodopa became necessary was extended by 2.5 years in the group receiving alpha-tocopherol and ascorbate. Results of this pilot study suggest that the progression of Parkinson's disease may be slowed by administration of these antioxidants. Controlled clinical trials using double-blind randomization techniques are required to confirm these results."

Fernandez- Calle et al compared serum levels of vitamin E between PD cases and controls and found no difference. They concluded that serum levels of Vitamin E played no part in the pathogenesis of PD.

1994

Lewitt compared vitamin E intake with the onset of PD in a group if patients and concluded:-

These results suggest that serum vitamin E concentrations do not play a role in the pathogenesis of PD.

1996

Offen et al published the results of recent research into neuroprotecton.

"We have found that the thiol containing compounds, reduced glutathione (GSH), N-acetyl-cysteine (NAC), and dithiothreitol (DTT) were markedly protective, while vitamins C and E had lesser or no effect. The thiol antioxidants and vitamin C but not vitamin E, prevented dopamine autooxidation and production of dopamine-melanin."

Morens et al compared Vitamin E intake with incidence of PD. Their findings:-

"these preliminary data do not conclusively document a beneficial effect of dietary vitamin E on PD occurrence "

1997

Lan and Jiang worked with MPTP Parkinson induced mice and found that:-

"(1) iron may induce neuronal damage and thus excessive iron in the brain may contribute to the neuronal loss in PD; (2) iron chelators and antioxidants (Vit E) may serve as potential therapeutic agents in retarding the progression of neurodegeneration."

2001

Roghani and Behzadi worked with Parkinsonian rats and found that repeated intramuscular administration of vitamin E exerts a rapid protective effect on the nigrostriatal dopaminergic neurons in the early unilateral model of PD.

2002

Zhang et al set out to examine the associations between intakes of vitamins E and C, carotenoids, vitamin supplements, and risk of PD. They assembled data for 76,890 women who were monitored for 14 years, and 47,331 men who were monitored for 12 years. 371 cases of PD were recorded. Their conclusions were:-

"Use of vitamin supplements and high intake of carotenoids do not appear to reduce the risk of PD. The reduction in risk of PD associated with high dietary vitamin E intake suggests that other constituents of foods rich in vitamin E may be protective. Alternatively, moderate amounts of vitamin E may reduce risk of PD, but this benefit may be lost with higher intakes."

2005

Etminan et al evaluated the results of 8 previous epidemiological studies and concluded that dietary vitamin E may have a neuroprotective effect attenuating the risk of PD. The studies did not suggest any protective benefits associated with vitamin C or beta carotene.

"We conclude that dietary vitamin E may have a neuroprotective effect attenuating the risk of PD. These results require confirmation in randomised controlled trials."