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Autopsy confirms that compound binds to amyloid plaque in human brain

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The autopsy of a man evaluated for dementia with Pittsburgh compound B has revealed for the first time that the imaging agent binds to the protein in amyloid plaques that characterize Alzheimer’s disease in the human brain. The findings come from a study by researchers at Massachusetts General Hospital that appeared in the March issue of Archives of Neurology.

The autopsy of a man evaluated for dementia with Pittsburgh compound B has revealed for the first time that the imaging agent binds to the protein in amyloid plaques that characterize Alzheimer's disease in the human brain. The findings come from a study by researchers at Massachusetts General Hospital that appeared in the March issue of Archives of Neurology.

The autopsy confirmed the diagnosis of dementia with Lewy bodies and produced several findings characteristic of Alzheimer's disease. But, while some plaques that typify Alzheimer's were seen, most amyloid-beta was found in the walls of blood vessels, a condition known as cerebral amyloid angiopathy.

"The distribution of amyloid seen at autopsy matched the overall distribution seen in the Pittsburgh compound B (PIB) imaging study; levels were higher in the cerebral cortex than in other areas of the brain," said coauthor Dr. Matthew Frosch of the MassGeneral Institute for Neurodegenerative Diseases. "Features of Alzheimer's pathology, amyloid plaques and neurofibrillary tangles, were observed, but not at a level that would support a separate diagnosis of Alzheimer's disease."

The researchers noted that, while their results confirm that uptake of PIB indicates the presence of amyloid in the brain, a positive PIB-PET scan cannot be equated with a definitive Alzheimer's diagnosis.

Previous PIB studies have shown that about 15% of control participants with no cognitive impairment have some level of PIB uptake. While the MGH report validates PIB as an imaging agent that binds to amyloid-beta deposits, it also indicates that interpretation of PIB-PET needs to be done in the context of a patient's clinical symptoms and other diagnostic studies, according to senior author Dr. John Growdon, director of the MGH Memory Disorders Unit.

Researchers also noted that it will be important to see how closely PIB-PET scans can track effects of drugs yet to be developed for removing amyloid from the brain or preventing its accumulation.

For more information from the Diagnostic Imaging archives:

PET tracer exploits new way to characterize dementia

Study taps cerebrospinal fluid to identify dementia

Amyloid plaque suggests fast onset of Lewy body dementia

Imagers seek answers for Alzheimer's diagnosis

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