Prevention and Treatment of Alzheimer's Disease

Medication may not be the only way to help prevent and treat this frightening disease.

| September/October 2002

Losing one’s mind, or “going senile,” may be the most feared consequence of aging. Only a few decades ago, it was widely assumed that this loss of mental capacity—also called dementia—resulted from a progressive hardening of the arteries that is an inevitable part of the aging process. According to this theory, once a person reaches a certain age their arteries will get so hard and narrow that they can no long provide brain cells with an adequate supply of oxygen. These delicate cells then begin dying off at the rate of tens of thousands per year. Eventually, the person loses so much of their brain tissue that their ability to think and remember becomes seriously impaired.

Scientific studies have indeed confirmed that diseased blood vessels are more likely to become clogged, resulting in strokes, which can in turn lead to a deterioration in cognitive function. Although this mechanism does play a role in many cases of memory loss and senility, extensive research conducted over the last twenty years has revealed that the vast majority of cases—at least 75 percent—of age-related dementias result instead from a chronic neurodegenerative disorder called Alzheimer’s disease (AD). Once considered to be a rare and mysterious condition, it is now recognized that AD is responsible for a rapidly growing epidemic of dementia in this country and around the world. Current estimates are that AD affects about 4 million Americans. Given that the elderly population is rapidly increasing and that AD strikes up to 50 percent of people aged eighty-five and older, the number of afflicted people is expected to triple in the next thirty to forty years.

Unfortunately, the discovery that AD and not hardened arteries is the culprit behind age-related dementia has led to an increase in our collective anxiety. This is reflected throughout the medical literature on AD, where an attitude of gloom and doom prevails. AD is not well understood, it’s difficult to diagnose, and it’s even more difficult to treat. Most people die from it within eight to ten years after the diagnosis is made. At least there have been concerted efforts to educate the public about how to prevent and treat hardened arteries, but with AD, very little information has been disseminated about the role of lifestyle factors in prevention and treatment.

Conventional Alzheimer’s therapy

The mainstay of conventional therapy for AD involves the use of a class of prescription drugs called cholinesterase inhibitors. These drugs work by blocking an enzyme that breaks down acetylcholine, one of the primary chemicals that the brain uses to store memories. Because acetylcholine is depleted in the brains of people with AD, taking a substance that increases it can potentially enhance or restore short-term memory and cognitive function. Currently available drugs in this category include tacrine, donepezil, rivastigmine, and galantamine.

Interestingly, galantamine, the newest drug to achieve approval for treatment of AD in the United States, is an extract from daffodil bulbs (Narcissus tazetta).

Despite the promise offered by these drugs, their effects have been modest at best. Although regular use can lead to mild improvements in mental function and behavior for 30 to 50 percent of patients, this only lasts for an average of two years. Once the drug stops working, the person’s condition tends to rapidly deteriorate. In other words, all these drugs do is buy time by keeping symptoms at bay. And, at an average cost of $4 per day, they do so at a steep price. They can also cause numerous side effects including nausea, vomiting, sweating, watery eyes, increased salivation, and diarrhea. Tacrine, the first drug to be routinely prescribed for AD, was later found to cause severe liver damage in a number of patients. Consequently, tacrine has largely been supplanted by its successors.

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