Australian researchers have used PET with Pittsburgh Compound B (PIB) to establish a correlation between the progressive accumulation of beta-amyloid plaque in the brain and cognitive deterioration associated with mild cognitive impairment and Alzheimer’s disease.
Australian researchers have used PET with Pittsburgh Compound B (PIB) to establish a correlation between the progressive accumulation of beta-amyloid plaque in the brain and cognitive deterioration associated with mild cognitive impairment and Alzheimer's disease.
PIB-PET studies at Austin Hospital's Centre for PET in Melbourne, Australia, involving 150 subjects who underwent psychometric memory tests, show that beta-amyloid plaque is related to the fundamental cause of Alzheimer's disease, according to nuclear medicine director Dr. Christopher C. Rowe.
His group's study of 44 Alzheimer's patients, 44 subjects with MCI, and 34 normal controls demonstrated that PIB-PET detects the early pathological changes of Alzheimer's disease long before the development of dementia. Rowe spoke at the 2007 SNM meeting in Washington, DC.
The trial compared results from two memory tests performed on the subjects with the mean standard uptake values of PIB in the frontal, posterior cingulate, parietal, lateral temporal, and occipital regions of their brains. PIB specifically targets beta-amyloid plaque. Cortical PIB binding correlated with the level of cognitive impairment. It was observed in all Alzheimer's patients, 60% of subjects with measurable cognitive deficits, and 20% of healthy volunteers.
When the groups were examined separately, however, only the MCI group showed a correlation with cognition. The results suggest that beta-amyloid plaque accumulation plays a pathogenic role in the progression from MCI to Alzheimer's disease, but its relationship with deteriorating cognitive skills is lost in the later stages of Alzheimer's disease as dementia develops.
"Our findings show that beta-amyloid is associated with brain dysfunction, even in apparently normal elderly individuals, providing further evidence that it is likely related to the fundamental cause of Alzheimer's disease," Rowe said.
Amyloid plaque buildup could precede Alzheimer's by up to 10 years, according to Rowe. Besides their implications for early diagnosis, the findings open a window of hope for individuals with minimal cognitive impairment who could benefit from early treatment.
Clinical trials should focus on monitoring response to anti-beta-amyloid treatments, he said.
The findings also have implications for anti-amyloid drugs now in clinical trials.
"If these prove successful, amyloid imaging will have a vital role in identifying those in need of treatment to prevent the development of Alzheimer's dementia," Rowe said.
In a different study, researchers from the Institute for Neurodegenerative Disorders in New Haven tried the agent iodine-123 IMPY as an amyloid plaque biomarker in eight patients with Alzheimer's and healthy subjects. Their findings suggest the agent could also play a role in the early detection of Alzheimer's, but more studies are needed to validate their assertion.
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