"For example," added Dr. Klunk, "we will be able to study families with a genetic makeup that leads to AD in half the family members at an early age, often in their 40's. Looking at these at-risk, presymptomatic subjects will show us if the plaques responsible for destroying the brain's ability to think and remember are present years before the first symptoms appear, or if they accumulate over a relatively short time period."
Knowing when the plaques begin to form is a key step in researching drugs that could have a real impact on the disease, said Dr. Klunk. "We will not only find out when plaques begin to form, we will be able to see directly if a medication is preventing or reversing plaque formation over the long term."
While the trial looked at a relatively small sample, 16 patients diagnosed with probable AD and nine control subjects, the results were highly significant. PET images showing PIB retention in the AD patients revealed PIB "stuck" to amyloid in areas of the brain known to contain these plaques, but not in areas of the brain where it is known that AD patients have low concentrations of plaques. PIB was not retained in the brains of eight of the nine control subjects, raising the possibility that the remaining control was starting to develop amyloid before any symptoms of dementia were apparent.
"These results are a very strong indicator of PIB's usefulness in providing quantitative information on amyloid deposits in the living brain," said Dr. Mathis.
In addition to Drs. Klunk and Mathis, the team included researchers from Uppsala University and PET Centre/Uppsala Imanet AB in Uppsala, Sweden; and the Karolinska Institute and Huddinge University, Stockholm, Sweden.