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Alzheimer's patient is taking her chances in clinical trial

A Pasadena woman undergoes surgery with no guarantee of treatment or positive results. She's scared, but there isn't much she can do as scientific advances have been slow.

July 04, 2010|By Shari Roan, Los Angeles Times

Gloria Lucio had two pencil-sized holes drilled into her skull in April, part of a procedure to possibly combat her Alzheimer's disease.

The surgeon may have injected an experimental gene therapy drug deep into her brain. Or, after months of tests, consultations and preparation, the Pasadena woman may not have received any treatment at all.

The willingness to endure such a surgery for a clinical trial with no guarantee of treatment seems extraordinary. But Lucio and her husband, Don Jones, acknowledge a biting reality: Even if she did get the drug, it may not work.

The substance that may have been injected — a virus carrying genes intended to produce a chemical called nerve growth factor — looked promising in a preliminary trial, but so have many other now-failed treatments.

Such are the options for someone with Alzheimer's disease in 2010.

The Alzheimer's Assn. recently estimated that cases of the neurological disease, which now affects about 5 million Americans, will more than double in the next 40 years — at enormous personal, social and economic costs.

The report was the latest in a drumbeat of dismal news about Alzheimer's. In March, a Phase 3 clinical trial of the promising drug Dimebon failed to produce positive results — another highly anticipated experiment gone bust. Medications currently in use can only mitigate early symptoms; none have been found to slow the disease.

"There's a feeling of desperation, not only among people with Alzheimer's disease or mild cognitive impairment but also with their family caregivers," said Gail Hunt, president of the National Alliance for Caregiving.

But behind the gloomy headlines, researchers say they know more about the cunning illness than ever before. They're developing techniques to identify it in its earliest stages, and within the next decade they expect treatments to slow or forestall the disease.

Given the swelling numbers of those afflicted, any advance can't come too soon.

"I want to get well," Lucio said on a rainy morning, a few days before her April surgery. "I want my brain to be healthy. But I'm scared. The holes — how big will they be?"

Her son, Valentin, 18, was sitting nearby. He points to the tip of his pinkie finger. "The holes are this big, Mom."

She nodded, still worried.

Lucio was reluctant to undergo the experimental treatment but, with a clear understanding of the situation, felt she had no choice. The disease had been making steady advances for years, quietly stealing pieces of her identity.

A former nurse-practitioner and political activist, she was afflicted with Alzheimer's at an earlier age than most patients. Lucio is homebound now and no longer fixes meals or pays bills. Her short-term memory is a sieve, and her husband and son don't leave her alone for long.

"How old are you?" she is asked.

"Sixty-eight," she said, somewhat hesitantly.

She is 57.

"How big are the holes?" she asked again.

Valentin crossed the room and gently touched the sides of his mother's head with his fingers as rain pounded on the picture window next to her chair.

"They'll be this size, Mom. They'll be right here."

Scientific developments

The predominant theory for the cause of Alzheimer's is a buildup of two types of proteins in the brain: beta-amyloid and tau. Scientists believe that plaques of beta-amyloid (which accumulate between nerve cells) and tangles of tau (which build up inside nerve cells) block the cells' ability to communicate and ultimately destroy them.

But the disease process is now thought to begin far earlier than anyone suspected — as long as 15 years before symptoms appear. In a study published in December in the Archives of Neurology, researchers found amyloid deposits in the brains of people who had no symptoms of dementia but later developed Alzheimer's.

Such knowledge is changing efforts to fight the disease.

"I think that the impact of the treatments is likely to be greater if we use them earlier," said Dr. Paul Aisen, director of the Alzheimer's Disease Cooperative Study at UC San Diego. "For disease-modifying treatments, a late stage may be too late to benefit."

Until recently, plaques could be verified only during an autopsy, so Alzheimer's diagnosis is based on highly subjective paper-and-pencil memory tests. That could change.

Biomarkers — physical signs of the disease — have been identified and are expected to soon replace memory tests. One detection method uses a PET scan with a radioactive chemical to detect beta-amyloid in the brain. Another measures tau and beta-amyloid proteins in spinal fluid.

Diagnosing and intervening earlier in the disease process, scientists predict, will bring about treatment successes.

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