Identifying Alzheimer's in Living Patients Jan. 10, 2001 -- UCLA researchers have developed an imaging technique that can identify the brain lesions responsible for Alzheimer's disease long before symptoms develop. If confirmed, the finding could lead not only to earlier diagnosis of Alzheimer's, but also to better ways to treat it.

The researchers combined a chemical marker they developed, called FDDNP, with positron emission tomography (PET) scanning to identify amyloid plaques and tangles in living patients. The plaques and tangles are believed to cause Alzheimer's by disrupting cell function and killing brain cells. But until now they could only be identified at autopsy.

In findings reported in the January issue of the American Journal of Geriatric Psychiatry, Jorge R. Barrio, PhD, and UCLA colleagues detected high concentrations of FDDNP in the memory centers of nine Alzheimer's patients who had been injected with the chemical marker prior to PET scanning. The findings were verified by brain autopsy in one patient who later died. High FDDNP concentrations were not seen in seven control subjects without Alzheimer's.

"We have developed the first tracer molecule that visually zeros in on the brain lesions caused by Alzheimer's disease," Barrio tells WebMD. "When Alzheimer's disease strikes, the memory center is the first location where plaques take root and destroy brain cells. So it is the first place where scientists must seek evidence of the disease."

The UCLA research team plans to study the technique in people who are at high risk for Alzheimer's disease but show no signs of dementia. They believe FDDNP will prove to be a sensitive chemical marker that can spot the disease long before symptoms occur.

Nearly 10% of people over the age of 65, and one in three people over 85, are believed to have Alzheimer's disease. It is estimated that 4 million Americans are afflicted with the progressive neurological disease and 19 million others are caring for someone who has it.

The condition often begins with mild memory lapses, then gradually advances to dementia. Patients with advanced disease become bedridden and lose most memory, language, and mental function.