Poor Visual Memory May Signal Alzheimer's

Second study shows gene therapy may provide new treatment for neurological disease

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MONDAY, Jan. 17, 2005 (HealthDayNews) -- Two new studies on Alzheimer's disease could lead to earlier diagnosis and more effective treatment for the mind-robbing condition, scientists say.

In the first study, researchers showed that diminished short-term visual memory, called iconic memory, may be an early indicator of an increased risk for Alzheimer's disease.

"People with mild cognitive impairment have very short visual memory," explained lead researcher Zhong-Lin Lu, a professor of psychology at the University of Southern California. "Visual memory is the first part of the memory system, and for people with mild cognitive impairment, their short-term visual memory almost does not exist."

The research appears in this week's issue of the Proceedings of the National Academy of Sciences.

In their study, Lu and his team tested iconic memory in 16 people, aged 65 to 99. All had mild cognitive impairment. During the test, the people were briefly shown a computer screen that had letters placed in various places on the screen. After looking at the screen for a moment, the people were asked to tell the researchers the position of each letter.

The researchers found that compared with younger or older people without cognitive impairment, the iconic memory in those with mild impairment faded faster. "Many of these subjects will get Alzheimer's disease in the next 10 years," Lu said.

The researchers believe that, with further study, a screening test using iconic memory could be developed that would help determine a person's risk for Alzheimer's. "This measure could help us predict whether people will have Alzheimer's disease or not," Lu said.

Dr. Samuel Gandy, vice chairman of the Alzheimer's Association's National Medical and Scientific Advisory Council, said that "iconic memory really gives the promise of finding a psychological marker for someone who is destined to develop Alzheimer's disease long before there is any disability detectable."

Gandy noted that most of the markers for Alzheimer's disease that researchers have been looking for are genetic, or present in blood or spinal fluid. "Still, the most sensitive way of determining who is going to develop Alzheimer's disease is with neuropsychological testing," he said.

The problem with neuropsychological tests is that they only reveal abnormalities once there is obvious cognitive impairment that interferes with functioning, Gandy said.

"If the iconic memory test is really a harbinger of who is going to develop Alzheimer's, then that would identify people for drug trials or intervention at a point when they have no abnormality in their daily function and their ability to live and work independently. And that would be a real advance," Gandy said.

In the second study, scientists from Lilly Research Laboratories experimenting with mice found that an injection of human apoE2 genes into the hippocampus of mice that did not have an apoE gene could reduce the amount of amyloid-beta by 30 percent to 50 percent. Amyloid-beta is the peptide needed to form the plaque seen in the brains of Alzheimer's patients.

The researchers suggest that injecting the apoE2 gene may treat Alzheimer's by helping to reduce amyloid-beta and preventing the development of amyloid plaques.

"These results are better than expected," Gandy said, explaining that gene therapy for Alzheimer's has been viewed with some skepticism. It has not been clear where one would inject genes or how many injections it would take for gene therapy to be effective.

"The encouraging thing about this experiment is that a single injection gave fairly dramatic results in this mouse model," Gandy said. "This isn't ready for human application. What this gives is a glimmer of hope for gene therapy."

The second study appears in the same issue of the Proceedings of the National Academy of Sciences.

More information

The Alzheimer's Association can tell you more about Alzheimer's disease.

SOURCES: Zhong-Lin Lu, Ph.D., professor, psychology, University of Southern California, Los Angeles; Samuel Gandy, M.D., Ph.D., professor, neurology, director, Farber Institute, Thomas Jefferson University, Philadelphia, and vice chairman, National Medical and Scientific Advisory Council, Alzheimer's Association, Chicago; Jan. 17-21, 2005, Proceedings of the National Academy of Sciences

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