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Medicine: Slow, Steady and Heartbreaking

10 minute read
Claudia Wallis

Alzheimer’s disease is a devastating illness of advancing age

“You look inside your mind and see nothing but black.”

—A victim

The first signs are small, puzzling and all too easy to dismiss. For Chicago Journalist Charles Leroux, it was his mother’s diminishing ability to manage her checkbook and count change. For Frank Holmes, a retired Boston businessman, it was the wild spending sprees by his once prudent wife and her increasing tendency to garble phone messages. For Eleanor Zimmerlein, an Illinois farmer’s wife, it was the decline in the quality of her husband’s handiwork: “Suddenly the row of shingles he’d put on the roof would be crooked, and he couldn’t saw a straight line.” And for Chicago Office Clerk Eleanor Marzillo, it began with her husband’s difficulty in shaving; first his trim mustache got bushier and bushier, then one day he shaved half of it off. At the same time, Marzillo recalls, rags were mysteriously collecting in the family car. “I couldn’t figure out what Tony was doing with these rags,” she says. “It turned out he knew how to start the car and how to drive, but he couldn’t figure out how to use the windshield wipers or defroster any more.”

Aberrations such as these mark the onset of Alzheimer’s disease (AD), the insidious and heart-breaking malady of advancing age. The memory lapses, confusion and dementia inevitably get worse. The intelligent and athletic Mrs. Holmes, now 65, forgot how to cook: she set a chicken ablaze by trying to roast it over all four burners of her stove. She also forgot how to play tennis and ultimately she had trouble recognizing her friends. Once an active Y.M.C.A. employee, Tony Marzillo, 61, gradually lost all ability to care for himself, becoming incontinent, unruly and destructive. “It was like chasing a 6-ft.-tall toddler around,” his wife recalls, “except you knew that a toddler would eventually learn the rules of the house.” Today both Marzillo and Holmes are institutionalized. Says Eleanor Marzillo of her husband: “He cannot speak, he cannot eat, he cannot ask for water.”

The relentlessness of Alzheimer’s disease makes it a nightmare for families of the patients. The affliction’s rising incidence threatens to make it a nightmare for the country at large. By far the leading cause of mental deterioration among the elderly, AD affects between 5% and 10% of all people over 65. Among them: former Movie Star Rita Hayworth, 64. Because most AD patients must eventually be placed in institutions, the disease puts tremendous demands on the nation’s health-care resources. Alzheimer’s victims constitute 50% to 60% of the 1.3 million people in nursing homes, accounting for more than half of the $25 to $26 billion spent annually on such care.

The disease will become more common and take an even greater toll as the U.S. population continues to age. On July 1, the U.S. reached a milestone: for the first time there are more Americans over 65 (27.4 million) than teen-agers (26.5 million). In March, Health and Human Resources Secretary Margaret Heckler created a special AD task force and proposed to increase federal funds for AD research to $25 million in 1984, up from $17 million in 1981. Says Heckler: “Every breakthrough we achieve is a step toward the reuniting of families and friends, the lifting of the veil of confusion and isolation from Americans who deserve days and years of celebration in their final years, not days and years of drift.”

Alzheimer’s disease was first identified in 1906 by German Physician Alois Alzheimer. His patient, a 51-year-old woman, suffered loss of memory, disorientation and later, severe dementia. After her death, Alzheimer conducted an autopsy on her brain and found the two distinctive characteristics of the disease: tangled clumps of nerve fibers and patches of disintegrated nerve-cell branches. Because Alzheimer’s patient was relatively young, AD was at first considered a disease of middle age; similar symptoms in elderly people were simply regarded as a natural consequence of aging. Today this view has been discarded. Even in an octogenarian, severe mental confusion “is a disease, not a natural decline,” says (Catherine Bick, acting deputy director of the National Institute of Neurological Communicative Disorders and Stroke (NINCDS).

Little real progress has been made in the treatment of AD since Alzheimer’s day, and even diagnosis remains difficult. The only way to be absolutely certain that a patient has the disorder is to examine the brain after death. Thus, the diagnosis must be approximated by a careful process of elimination. Through CAT scanning and other tests, the physician gradually determines that the patient has not suffered a series of small strokes, does not have Parkinson’s disease, a brain tumor, depression, an adverse drug reaction or any other possible cause of dementia. If all tests are negative, AD is diagnosed by default. This conclusion may be further verified with psychological tests.

Alzheimer’s disease would be far easier to treat and detect if doctors knew what caused it. The fact that the disease often occurs in several members of the same family suggests that a genetic factor is at work. This factor “is most prominent in very early onset cases,” says University of Minnesota Psychiatrist Leonard Heston.

In one family, for instance, two out of three siblings developed Alzheimer’s by age 27. According to Johns Hopkins Psychiatrist Marshal Folstein, a sibling or child of an AD victim runs a greater than 50% chance of developing the disease by age 90. Still, heredity alone cannot explain the disease, which often affects individuals whose families have no history of the disorder. “Possibly it comes down to genetic susceptibility triggered by one or more things,” suggests Bick of NINCDS. Some doctors speculate that the trigger may be a slow-acting virus, similar to the “slow viruses” that cause such rare brain disorders as kuru and Creutzfeldt-Jakob disease in man, and scrapie in sheep and goats. Unfortunately, all efforts to isolate an AD virus have failed. Concludes Virologist Joseph Gibbs of the National Institutes of Health: “If slow viruses are involved in Alzheimer’s, I suspect that the association is remote.”

Other researchers are looking into the role of aluminum in causing AD. In 1973 a University of Toronto team reported finding ten to 30 times the normal concentration of the metal in the brains of autopsied AD victims. The finding was provocative, since animals can develop neurofibrillary tangles similar to those found in AD patients when given aluminum salts. The role of aluminum remains unclear, however, and doctors now say that cooking in aluminum pots could not cause AD.

Answers to the Alzheimer’s puzzle will probably come from research into the chemistry of the brain. By far the most promising lead was found in 1977, when scientists in Britain reported that AD victims have only one-tenth the normal level of an enzyme needed to produce acetylcholine (ACh). That chemical plays a vital role in the transmission of nerve signals, particularly for such higher functions as memory and learning. The deficiency appears to be due to acute damage to the nucleus basalis, a tiny structure deep in the forebrain that produces ACh. A team at Johns Hopkins, headed by Neuropathologist Donald Price, found that up to 95% of the nerve cells in this area of the brain are destroyed in AD patients. Says Price: “You can see the difference with a naked eye.”

Unfortunately, ACh cannot be supplied directly to patients because it breaks down in the digestive tract. Doctors have tried to get around this problem by treating AD patients with choline and lecithin, chemicals that the body uses to make ACh. In doing so they take their cue from the treatment of Parkinson’s disease, a neurological disorder that often responds well to L-dopa, a substance necessary for the production of the neurotransmitter dopamine, which Parkinson’s patients seem to lack. Researchers have also tried treating AD with physostigmine, a substance that prevents the breakdown of ACh. In all cases, the results are inconclusive. Though some patients have experienced limited, short-term improvements in memory and cognition, such therapy “does not appear to be the L-dopa for Alzheimer’s,” says Thomas Chase, a NINCDS researcher.

Scientists are experimenting with a number of other treatments for AD. Among them: piracetam, a drug used by European doctors to treat memory disorders, head injuries and learning disabilities in children; and naloxone, a chemical that blocks the action of opiate-like substances in the brain. The results so far are not encouraging. Admits Price “There is no effective therapy.”

One possible problem is that the therapy comes too late. By the time AD is diagnosed, too many brain cells may have died for the process to be reversed. “If we can come up with better diagnostic procedures, it might be possible to block the progress of AD chemotherapeutically in the next five years.” says Gibbs of NIH One promising method is a new scanning process called PET (positron emission tomography), which measures glucose metabolism in living cells. PET-scan studies by Dr. David Kuhl of U.C.L.A., among others, have revealed drastic decreases in metabolism in the brains of AD patients. Kuhl hopes to develop an early diagnostic test so that AD patients can “receive treatment while their brains are still healthy and not mush.”

Until better tests and drug therapies are available, doctors treating Alzheimer’s patients stress teaching them and their families how to cope. Such advice is now available in 31 states through the Chicago-based Alzheimer’s Disease and Related Disorders Association. In addition, many hospitals have established AD support groups, and there are special clinics that work closely with patients, such as the Burke Rehabilitation Center in White Plains, N.Y.

A great deal can be done to improve the quality of life for AD patients and their families, according to Johns Hopkins Gerontologist Nancy Mace. She is co-author with Johns Hopkins Psychiatrist Peter Rabins of The Thirty-Six Hour Day, a tellingly titled book on the grueling aspects of caring for the victims. Most important, she explains, is to “simplify the sensory information the patient is getting.” Mace suggests discussing only one topic at a time, not confusing patients with too many choices, posting instructions on how to use household appliances and encouraging the individual to make lists and written reminders. No one with Alzheimer’s should be cut off from friends or a normal routine, Mace argues. But instead of having a lot of people over for dinner, only one or two should be invited at a time. Physical activity should be encouraged to stimulate the appetite, prevent muscle contracture and bone fractures and promote sleep.

It was once thought that severely demented AD patients could not live very long. Today, says Chicago Neurologist Jacob Fox, they can survive for upwards of 15 years. “We’ve gotten better at preserving lives,” he says, “but it’s not clear we’re doing the person a favor.” Understandably, Alzheimer’s patients can suffer severe depression. Their families may suffer even more. In addition to the enormous costs of health care and institutionalization, which is generally not covered by Medicare or private insurance, there is the terrible, haunting sense of loss to family members of the person who is still with them.

“Everyone talks about guilt feelings when they have to institutionalize a person they love,” says Frank Holmes, the retired Boston businessman whose wife is in a nursing home. “It’s not guilt I feel, it’s heartbreak.” —By Claudia Wallis. Reported by J. Madeleine Nash/Chicago and Sue Wymelenberg/Boston

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