Alzheimer technique showcases imaging progress
If Time magazine featured a "molecule of the year," one strong contender would be Pittsburgh compound B, a cleverly designed tracer that highlights a hallmark Alzheimer protein in a positron emission tomography (PET) brain scan.
According to a report in the February Archives of Neurology, preliminary data on Pittsburgh compound B look so promising that the molecule now serves as a model of progress toward imaging abnormal brain deposits linked to specific diseases.
Development of Pittsburgh compound B was supported through grants from the Alzheimer's Association, the National Institute on Aging and the National Institute of Mental Health.
"The ability to link sophisticated chemistry with modern imaging techniques holds great future promise, and watching Pittsburgh compound B move from the laboratory through animal studies and into its first human trials has been extremely heartening and inspiring," says William H. Thies, Ph.D., Alzheimer's Association vice president, medical and scientific affairs. "We've had an opportunity to follow a top research team through the whole scientific process from concept to clinic. We're proud to have supported this work and hope the news remains good as we move into larger human trials."
Beta-amyloid, the protein fragment highlighted by Pittsburgh compound B, is a prime suspect in Alzheimer-related brain cell damage and destruction. The fragment is clipped from a larger parent molecule and accumulates by stages into the amyloid plaques considered one hallmark of the Alzheimer brain.
Several experimental drugs targeting beta-amyloid are under development. In some studies in the early stages of human clinical trials, imaging with Pittsburgh compound B is being included as part of the experimental protocol.
Larger-scale Pittsburgh compound B studies are also planned to clarify whether beta-amyloid occurs in the normal brain; whether there is a predictable pattern of increasing deposition as Alzheimer's disease progresses; whether patterns of deposition can be tied to memory problems and other Alzheimer symptoms; and whether symptoms improve when beta-amyloid levels are reduced. Answering these questions could significantly accelerate drug development.
Preliminary success with Pittsburgh compound B is raising interest in designing molecules that could highlight characteristic protein deposits associated with other degenerative brain diseases, including Parkinson's and dementia with Lewy bodies.
For more information, please see:
- Alzheimer's Association fact sheet on drugs targeting beta-amyloid and the "amyloid hypothesis"
- A Jan. 24, 2004 Alzheimer's Association Research News feature on the first human trial of Pittsburgh compound B