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It has been proven that people with Alzheimer's lack or have a shortage of a chemical called Acetylcholine [a-see-til-KOH-leen] which is essential to maintaining communications between the brain cells responsible for memory. However, increasing the amount of acetylcholine in the brain will only slow the progression of Alzheimer's, not reverse it. Acetylcholine is scarce in Alzheimer's patients because the brain cells that release it are essentially shriveling up and dying. Estrogen (British: oestrogen) therapies hold some promise to stop the degenerative process. According to a small-scale study conducted in 1996 by the Veterans Affairs Dept. and the University of Washington, women with Alzheimer's who were given estrogen for two months showed significant improvements in memory and attention, which diminished when they stopped taking it. And epidemiological research indicates that women who have estrogen-replacement therapy after menopause are less likely to develop Alzheimer's. Several drugs have been developed to increase the amount of Acetylcholine. All of these drugs have side effects, including nausea and vomiting. However, there is another approach. Glutamate is the main excitatory neurotransmitter in the brain. It is believed that too much stimulation of nerve cells by glutamate may be responsible for the degeneration of nerves that occurs in some neurological diseases such as Alzheimer's disease. A drug called Memantine (retail name: Namenda) decreases the effects of glutamate. Tacrine (Cognex) is not generally prescribed in USA/Canada, because of liver damage; other drugs are preferred.
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