- The Washington Times - Wednesday, December 20, 2006

California researchers have developed a new imaging compound that can detect and map tangles and amyloid plaques — the telltale signs of Alzheimer’s disease — in the brains of patients with mild cognitive impairment, a condition that increases the risk of the disease.

“This study suggests we may now have a new diagnostic tool for detecting pre-Alzheimer’s conditions to help us identify those at risk, perhaps years before symptoms become obvious,” said Dr. Gary Small, lead author of the study published in the Dec. 21 issue of the New England Journal of Medicine.

Dr. Small, a professor of psychiatry and Parlow-Solomon professor on aging at UCLA, said he foresees opportunities for using this technology, if approved by the Food and Drug Administration, for “testing novel drug therapies” and being able to see if they counter progression of Alzheimer’s before the brain is damaged.

He said that someday “we could be managing levels of tangles and plaques like we now manage cholesterol.”

The multimillion-dollar study was funded in part by the National Institute on Aging and the U.S. Administration on Aging, Dr. Small said. The 14 researchers who assisted him are all from UCLA.

The new imaging molecule, called FDDNP, which he and several others involved in the research invented, binds to both abnormal tangle and plaque deposits and can be seen on PET (positron emission tomography) scans, which are used mostly to view cardiovascular disease and cancer.

Up until now, it’s largely taken autopsies to confirm the presence of tangles and plaques in Alzheimer’s patients, as well as Alzheimer’s diagnoses.

But Jorge Barrio, professor of medicine and medical pharmacology at the David Geffen School of Medicine at UCLA, another author, said by using FDDNP, his team saw “the definitive pattern [of tangles and plaques] starting early in patients with mild cognitive impairment and advancing in those with Alzheimer’s.”

The study included 83 volunteers ages 49 to 84, who reported having memory problems and who had undergone neurological and psychiatric evaluation and PET scanning of the brain.

Based on cognitive testing, 25 were classified as having Alzheimer’s, 28 as having mild cognitive impairment and 30 as normal.

PET scans were performed on the volunteers after they were injected with FDDNP.

With FDDNP, the imagery showed that in more advanced cases of mental decline, there were higher concentrations of the new molecule in areas of the brain where tangles and plaques tend to accumulate. Patients with Alzheimer’s also had the most FDDNP binding, which indicates they had higher levels of the abnormal proteins.

The presence of those deposits in the brain were described in the first Alzheimer’s diagnosis, which occurred in Germany nearly a century ago.

Follow-up FDDNP-PET scans on 12 patients two years later found that those who underwent a decline in mental function during the period showed a 5 percent to 11 percent increase in FDDNP binding than had been shown on earlier scans.

Dr. Richard J. Hodes, director of the National Institute on Aging, estimates that 4.5 million Alzheimer’s patients live in the United States. That figure could triple by 2050.

“We urgently need techniques to see brain changes in the earliest stages of cognitive decline, so we can identify people at risk and test drugs to stop or slow the progression of Alzheimer’s,” he said.

The UCLA researchers want to conduct a large clinical trial to assess further the benefits of their discovery.

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