The most characteristic features of Alzheimer's disease are senile plaques of beta-amyloid peptide, neurofibrillary tangles involving tau protein, loss of synapses, and (ultimately) the death of neurons. Although neurofibrillary tangles are more closely associated with neuronal death than beta-amyloid, the evidence is becoming convincing that beta-amyloid is the factor most responsible for starting the degenerative processes of Alzheimer's disease.
Researchers have shown that cultured cells are prevented from beta-amyloid toxicity with the addition of vitamin E (Grundman 2000). Researchers at the University of Kentucky published a ground-breaking article showing that vitamin E prevented the increase of polyamine metabolism in response to free-radical mediated oxidative stress caused by the addition of beta-amyloid to the rat neurons (Yatin et al. 1999).
Research conducted in Germany showed that both natural and synthetic vitamin E were more effective than estrogen (17-beta estradiol) in protecting neurons against oxidative death caused by beta-amyloid, hydrogen peroxide, and the excitatory amino acid glutamate (Behl 2000).
Research conducted at the University of California, San Diego, School of Medicine studied the protective effects of vitamin E in apolipoprotein E-deficient mice. Those treated with vitamin E displayed a significantly improved behavioral performance in the Morris water maze. Also, the untreated mice displayed increased levels of lipid peroxidation and glutathione, whereas the vitamin E-treated mice showed near normal levels of both lipid peroxidation and glutathione (Veinbergs et al. 2000).
A study of 44 patients with Alzheimer's disease and 37 matched controls showed that vitamin E levels in the cerebrospinal fluid (CSF) and serum were significantly lower in Alzheimer's patients (Jimenez-Jimenez et al. 1997).
In the Alzheimer's Disease Cooperative Study, 2000 mg of vitamin E were given to Alzheimer's disease patients. This slowed the functional deterioration leading to nursing home placement (Grundman 2000).
An article by Sano et al. (1997) described a double-blind, placebo-controlled, randomized, multicenter trial of patients with Alzheimer's disease of moderate severity. A total of 341 patients received the selective monoamine oxidase inhibitor selegiline (10 mg a day), alpha-tocopherol (vitamin E, 2000 IU a day), both selegiline and alpha-tocopherol, or placebo for two years. The baseline score on the Mini-Mental State Examination was higher in the placebo group than in the other three groups. Both vitamin E and selegeline delayed the progression of the disease with vitamin E acting slightly better than selegeline (median time 670 vs. 655 days, respectively).