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Amyloid plaque suggests fast onset of Lewy body dementia

(PSYCHIATRIC TIMES) - An early 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.

Dr. Christopher Rowe, director of nuclear medicine at Austin Hospital in Melbourne, Australia, drew that preliminary conclusion from a study of 29 subjects:

* seven patients with dementia with Lewy bodies (DLB)

* seven with Alzheimer's disease

* two with mild cognitive impairment (MCI)

* one with Parkinson's disease

* two with frontotemporal dementia

* 10 normal controls

Results of Rowe's trial, presented in June at the 2005 Society of Nuclear Medicine meeting, went beyond simply comparing the uptake patterns of C-11 Pittsburgh compound B (PIB), as was originally intended. Rowe and colleagues found evidence pointing to a direct relationship between the amount of amyloid deposition and the rate of DLB progression.

A large amount of amyloid was measured with C-11 PIB, a PET probe targeted specifically to amyloid protein, in the brains of fast-developing fulminant DLB. Less amyloid appeared in the brains of slow-developing cases. These had a long prodromal phase of mild cognitive symptoms for five or more years before the characteristic clinical features developed, Rowe said.

Full-blown systems of fulminant DLB develop in one to two years after the first physical signs of the condition.

"It's still early, but our experience has been encouraging. It suggests that amyloid may have an accelerant role in the development of this condition," he said.

Amyloid protein is a suspected cause of Alzheimer's disease, but its influence on the genesis of DLB is not known. Neurofibrillary tangles, commonly associated with amyloid plaques in the brain of an Alzheimer's patient, do not appear in DLB cases, Rowe said.

DLB is responsible for 20% of dementias, making it second only to Alzheimer's as a cause of cognitive degeneration. Like Alzheimer's, DLB is difficult to diagnose. Symptoms involve visual hallucinations, cognitive impairment, and parkinsonian features such as rigidity and bradykinesia. The diagnostic specificity of a physical examination is about 85%, but sensitivity may be as low as 45%, Rowe said.

In the more advanced Alzheimer's and DLB cases, low cortical glucose metabolism measured with FDG-PET was present in areas that had high levels of PIB binding. This suggests a relationship between the presence of amyloid protein, directly measured with PIB, and neuronal dysfunction detected with FDG, he said.

Abnormal PIB patterns also appeared in the two subjects with MCI. In both cases, clinical history and neuropsychological tests revealed progressive decline, making it likely that Alzheimer's disease will develop, Rowe said. Three control subjects had positive PIB-PET tests, and one of those individuals subsequently progressed to MCI.

Generally, lower C-11 PIB uptake was seen in DLB patients than in the Alzheimer's disease subjects. The amount of frontal activity was less pronounced though still prominent. The seven DLB patients showed variable PIB binding, ranging from normal to the upper Alzheimer's disease range with slightly greater occipital binding and less posterior cingulate binding than in AD.

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