Molecular imaging aids Alzheimer?s diagnosis
Research presented at the SNM annual conference this week in New Orleans suggests that the use of molecular imaging in the management of neurodegenerative disease, particularly for very early diagnosis of Alzheimer’s disease (AD), will enable researchers to monitor disease progression, identifying those at risk and assessing the effectiveness of new therapies.

Using PET and the radiotracer Pittsburgh Compound-B (PiB), which is capable of binding to plaques found in the brains of AD patients, researchers at the University of Pittsburgh found that beta-amyloid plaque imaging could provide early detection of AD and more accurate differential diagnosis of other dementias by revealing the presence or absence of beta-amyloid plaques.

In a longitudinal study following participants for more than four years, the Pittsburgh research team sought to compare patients with AD to elderly control individuals and to subjects with mild cognitive impairment (MCI) to determine control subjects at risk of developing cognitive impairment and the MCI subjects who were most likely to progress on to a clinical diagnosis of AD. Thirty-five people (four with mild to moderate AD, 10 with MCI and 21 elderly controls) underwent PiB-PET scans at yearly intervals over four years.

“The research literature shows that 30 to 40 percent of people with MCI do not progress to AD during five to 10 years of follow-up testing,” said Chester Mathis, PhD, professor of radiology at the University of Pittsburgh, who presented the team’s findings. “Our hypothesis was that MCI subjects with brain plaque would develop AD and MCI subjects without plaque would not advance to AD.”

The researchers found that about 60 percent of the MCI subjects had plaque loads comparable to AD subjects, while about 35 percent of MCI subjects had no detectable plaque. After monitoring the MCI participants for four years, they found that only those with plaque progressed on to the clinical diagnosis of AD.

“In AD subjects, there appears to be a ceiling to plaque deposition, and plaque concentration does not increase as the disease progresses from mild to advanced stages of AD,” Mathis said.

The researchers also assumed that the elderly control group would have little PiB retention (indicating no amyloid deposits), but the results were otherwise.

“We found that about 25 percent of participants between 65 and 80 years of age had significant deposits of amyloid plaque in their brains,” Mathis stated. “We hypothesize that these control subjects are in a pre-symptomatic, at-risk state that will eventually lead to AD.”

According to the Alzheimer's Association, more than five million people in the United States have AD, and by 2050, that number could triple. Currently it is the seventh leading cause of death in the United States.