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(PSYCHIATRIC TIMES) - A human trial using PET imaging with carbon-11 Pittsburgh compound B suggests a relationship between the amount of brain-based amyloid found with the agent and the rate at which symptoms of dementia with Lewy bodies progress.

Amyloid protein is a suspected cause of Alzheimer's disease, but its influence on the genesis of dementia with Lewy bodies (DLB) is not known. Neurofibrillary tangles, commonly associated with amyloid plaques in the brain of an AD patient, do not appear in DLB cases. Like Alzheimer's, DLB is difficult to diagnose. The diagnostic specificity of a physical exam is about 85%, but sensitivity may be as low as 45%.

Dr. Christopher Rowe, director of nuclear medicine at Austin Hospital in Melbourne, Australia, and colleagues evaluated 29 subjects: seven with DLB, seven with AD, two with mild cognitive impairment (MCI), one with Parkinson's disease, two with frontotemporal dementia, and 10 normal controls.

The researchers, who presented their results at the Society of Nuclear Medicine meeting in June, went beyond their initial intention to simply compare the uptake patterns of C-11 Pittsburgh compound B (PIB). They found evidence indicating a direct relationship between the amount of amyloid deposition and the rate of DLB progression.

C-11 PIB, a PET probe targeted specifically to amyloid protein, measured a large amount of amyloid in the brains of fast-developing fulminant DLB, and less in the brains of slow-developing cases. The latter had a long prodromal phase of mild cognitive symptoms for five or more years before the characteristic clinical features developed. Full-blown symptoms of fulminant DLB develop one to two years after the first physical signs.

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