New Test May Allow Rapid Diagnosis of Alzheimer’s
A new skin test may allow rapid diagnosis of Alzheimer’s disease and may also be able to predict who will develop the disease, a finding that could make possible more effective treatment for the disorder.
Alzheimer’s, which affects as many as 4 million Americans, producing severe memory loss and eventually death, currently can be diagnosed only by excluding all other possible diseases.
“This discovery, if confirmed, could provide a big step forward in our efforts to deal with and understand the disease,” said Patricia Grady, acting director of the National Institute of Neurological Disorders and Stroke, where the research was conducted.
Researchers have been intensively seeking new diagnostic techniques to complement a number of potential treatments for the disease now being studied, such as the recently approved drug tacrine.
The hope is that these treatments will be much more effective if they are used in the early stages of the disease, but it has been impossible to test such a theory because of the inability of clinicians to identify Alzheimer’s victims at an early stage.
The test could also shield patients from the extensive and expensive testing now necessary for diagnosis in the advanced stages of the disease, saving hundreds of millions of dollars, Dr. Daniel L. Alkon of the National Institute of Neurological Disorders and Stroke reports in today’s issue of the prestigious Proceedings of the National Academy of Sciences.
Researchers may also be pointed in the direction of a whole new method of treating Alzheimer’s by a second report in the journal, this one by Dr. Carl W. Cotman of UC Irvine. Cotman and his colleagues report that a protein associated with Alzheimer’s, called beta-amyloid, causes brain cells exposed to it to commit suicide, a process known as apoptosis.
Apoptosis occurs naturally in the body to remove cells that are no longer needed, such as cells damaged or infected by viruses.
Researchers previously thought that beta-amyloid simply acted as a cellular poison, killing cells outright--a process that is theoretically very difficult to stop. But if Cotman is correct and the cells are dying by apoptosis, it should be possible to interfere with the process and thereby halt the progression of Alzheimer’s.
“This moves us in a more hopeful direction” for the development of new treatments, said the institute’s Dr. Irwin J. Kopin.
Alzheimer’s disease is the fourth-leading cause of death in the United States, following only heart disease, cancer and stroke. According to a Gallup survey released Tuesday by the Alzheimer’s Assn., one in every 10 adults in this country has a relative with the disorder and one in every three knows someone with it.
Caring for a victim exerts an “enormous emotional and financial toll” on relatives, said association president Edward Truschke. According to a recent UC San Francisco study, the average cost of such care is $47,000 per year, whether the patient is hospitalized or cared for at home.
JoAnn McConnell, senior vice president for medical and scientific affairs of the Alzheimer’s Assn., cautioned that much more work is necessary to understand the significance of both new developments.
“What we have here is not a breakthrough, but more pieces in the puzzle,” she said. “We’re learning better what’s causing the symptoms of Alzheimer’s, but we’re still working at trying to track down the actual cause.”
The cause of Alzheimer’s is unknown, but its most prominent characteristic is the formation of so-called plaques and tangles in the brain composed of beta-amyloid. The presence of these proteins, determined through an autopsy, is currently the only definitive way of diagnosing the disorder. Researchers still hotly debate whether the proteins are the cause of the disorder or simply a byproduct.
Although most researchers have concentrated on beta-amyloid, Alkon and his colleagues at the institute and the Cornell Medical Center in White Plains, N.Y., have taken a different tack. They have been studying another protein, called a potassium channel, because such channels play a key role in memory. The channel contains a microscopic hole that permits potassium to enter or escape brain cells and other cells.
The researchers found that skin cells of 15 Alzheimer’s patients had a defect in the potassium channels that could be easily measured, whereas skin cells from 35 healthy people had no such defect. The test is performed by removing cells from the skin or the nose and treating them with chemicals. If the potassium channels are normal, a microscopic spark is created that is easily detected. If the channels are damaged, no spark occurs.
Alkon conceded that the skin tests need to be studied in a much larger clinical trial but said that “with these statistics, it is extremely promising that the result will hold up in the population at large.”
Cotman’s research at UC Irvine was more conventional than Alkon’s because he was studying the effects of beta-amyloid. He found that when he injected specific fragments of the protein into brain cells grown in the laboratory, the cells exhibited all the biochemical and visual characteristics of apoptosis.
The importance of the discovery is that apoptosis is a process that is turned on and off throughout life. When the brain is formed in the fetus, for example, a large excess of brain cells are present. The shape and function of the adult brain are then created by cellular processes that trigger the suicide of the unwanted cells.
Because apoptosis can be controlled naturally by the body, it should be possible to control it artificially with drugs, Kopin said. Such drugs could be potent inhibitors of Alzheimer’s, he said.
