The PET imaging showed that the more advanced the disease, the higher the FDDNP concentrations in the temporal, parietal and frontal brain regions, where the abnormal protein deposits typically accumulate. Patients with Alzheimer's showed the most FDDNP binding, indicating a higher level of plaques and tangles than other subjects.

"We could see the definitive patterns starting early in patients with mild cognitive impairment and advancing in those with Alzheimer's disease," said Dr. Jorge Barrio, a study author and professor of medical and molecular pharmacology at the David Geffen School of Medicine at UCLA.


All subjects also received a PET brain scan using a more conventional chemical marker called FDG, which measures the metabolic function of cells and has previously been used in aiding diagnosis for Alzheimer's disease. However, FDG cannot identify the abnormal brain protein deposits that may cause the disease.

In addition, 72 subjects received magnetic resonance imaging (MRI) scans, which show brain structure and size.

Scientists found that the FDDNP–PET scan combination differentiated between study subject groups better than the FDG–PET combination or the MRI.

"FDDNP yielded excellent diagnostic accuracy and precisely predicted disease progression and brain pathology accumulation," said Barrio. "FDDNP–PET also delivers the promise of new drug monitoring in human subjects for a more rapid introduction of therapeutic candidates to control or slow progression of the disease."

Researchers performed follow-up scans two years later on 12 research subjects, using FDDNP–PET. Patients whose conditions had grown worse — declining from normal cognitive function to mild cognitive impairment or from mild cognitive impairment to Alzheimer's disease — showed a 5 to 11 percent increase in FDDNP binding over their previous brain scans, suggesting an increase in plaques and tangles.

A brain autopsy completed on a follow-up Alzheimer's patient who died 14 months later showed high plaque and tangle concentrations in areas that had previously demonstrated high FDDNP binding values on the PET scan.

"This is the first time this pattern of plaque and tangle accumulation has been tracked in living humans over time in a longitudinal study," said Small.

The study was funded by National Institutes of Health; the Department of Energy; General Clinical Research Centers Program; the Rotary CART Fund; the Fran and Ray Star Foundation Fund for Alzheimer's Disease Research; the Ahmanson Foundation; the Larry L. Hillblom Foundation; the Lovelace Foundation; the Judith Olenick Elgart Fund for Research on Brain Aging; the John D. French Foundation for Alzheimer's Research; and the Tamkin Foundation. Department of Energy funds supported FDDNP synthesis, which was performed at the UCLA Cyclotron Laboratory under professor Nagichettiar Satyamurthy's direction. No company provided support of any kind for this study.

More Industry Headlines