The Forgetting: Alzheimer's -- Portrait of an Epidemic by David Shenk, Doubleday, $24.95, 290 pages.
 



The News & Observer



September 23, 2001

A history of Alzheimer's disease


By Phillip Manning

When he was 63 years old, Ralph Waldo Emerson was still vigorous in body, but his mind was beginning to fail. Unlike most of us, he did not flinch from that reality. Instead, he wrote a poem called "Terminus," which began: "It is time to be old/To take in sail." A few years later, Emerson attended the funeral of his longtime friend Henry Wadsworth Longfellow. "The gentleman who lies here," Emerson reportedly said, "was a beautiful soul, but I have forgotten his name."

Emerson died in 1882, 15 years after he wrote "Terminus" and 25 years before Alois Alzheimer examined the brain of a deceased, deranged woman and lent his name to her condition. Consequently, we have no definitive diagnosis of Emerson's dementia, but it is almost certain that he was suffering from Alzheimer's disease, a horrific affliction that steals the mind.

In "The Forgetting: Alzheimer's: Portrait of an Epidemic," David Shenk offers a comprehensive look at the disease. He recounts its history and provides poignant tales of its sufferers -- including Emerson, Ronald Reagan and Jonathan Swift -- and of their caregivers, who tend loved ones who no longer recognize them. The author notes that Alzheimer's is becoming epidemic in America as life spans increase, and he recounts the stories of the scientists who are searching for a cure for the disease. The result of trying to cover so much ground is an ambitious but jumpy book that flits from topic to topic. Nevertheless, it is worthwhile reading for the millions of Americans whose lives have been scarred by Alzheimer's and for those who want to learn more about the disease. It also offers hope for the future.

One can find hope in the intensive research under way to find a cure for Alzheimer's. To develop remedies for most diseases, scientists must test experimental drugs on infected animals. Problem is, only humans suffer from Alzheimer's. Because the animals of choice for most medical experiments are mice -- which are small, easy to study and have short life spans -- scientists had to build a mouse that could get Alzheimer's.

This is a complex process, but Shenk explains it clearly. Researchers can build new strains of mice through a process called transgenics. Essentially, they "knock out" a snippet of DNA from one species and insert it into another. In 1996, Karen Hsiao at the University of Minnesota spliced a human gene into a mouse. Although normal at birth, the mouse developed amyloid plaques in its brain as it aged, similar to those found in humans with Alzheimer's. Memory problems ensued; the mouse forgot the path through mazes it had previously mastered. Now, the hunt was on to find a drug that would slow the growth of the deadly plaques in the knock-out mouse.

According to Shenk, the most promising treatment was developed by Dale Schenk at Elan Pharmaceuticals. Surprisingly, the breakthrough drug was a vaccine. Vaccines, such as those used for polio or mumps, work by injecting a weakened virus into the body. The virus stimulates the immune system, which then recognizes and attacks the real virus if it comes along. Researchers injected bits of a synthetic plaque-causing amyloid into the bloodstreams of knock-out mice. When the brains of the vaccinated mice were examined, scientists found fewer plaques than in unvaccinated mice. Even more remarkably, they found a substantial reduction in the plaques of elderly transgenic mice who were given the vaccine after the plaques had developed. The vaccine, Shenk writes, was "not just a shield but also an antidote."

Do we have a cure for Alzheimer's? Not yet. Many questions remain. The two big ones are: Will the vaccine prevent the formation of amyloid plaques in humans? And do the plaques themselves actually cause Alzheimer's, or are they merely a byproduct of the disease? Despite these questions, the vaccine has raised the hopes of victims, caregivers and researchers.

As our knowledge of Alzheimer's has grown, so have our methods of coping with it. Both caregivers and victims know better what to expect, and new drugs are on the way that may slow or stop its mind-killing progression. However, until effective treatments are available, the most pressing question facing sufferers, especially those in the early stages of the disease, is how best to face their fate. Shenk movingly explores this issue through the stories of Jonathan Swift and Emerson, two great intellects and writers who coped with the disease in entirely different ways.

Swift railed against the illness that was destroying his mind. He became withdrawn and hostile, alienating friends and family. As the disease progressed, Swift mourned the death of his intellect, and his last words were, "I am a fool."

Emerson, on the other hand, accepted what was happening to him. "He suffered very little," wrote his son Edward, "took nourishment well. ... He went to his study and tried to work, accomplished less and less, but did not notice it." Two weeks before he died, Emerson could still muster a smile, although he could not remember how to spell "Concord," the town where he had spent most of his life. By accepting his illness, Emerson avoided many of its terrible side effects, such as the loneliness and bitterness that consumed Swift.

The Emersonian approach of accepting the disease has modern disciples. Morris Friedell, a college professor from Santa Barbara whom Shenk interviewed, has Alzheimer's and is trying to transcend it. Friedell believes rehabilitation from Alzheimer's is possible. Get rid of mental and physical clutter, he advises. " 'Simplify, simplify, simplify,' -- just like Thoreau." Although Friedell hopes desperately that scientists will find a cure for the disease that is wasting his mind, he has managed to maintain his dignity in the face of its encroachments. And that, too, is reason for hope.

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