[11C] PIB-,[18F] FDG-PET and MRI imaging in patients with Parkinson's disease with and without dementia

P Jokinen, NM Scheinin, S Aalto, K Någren… - Parkinsonism & related …, 2010 - Elsevier
P Jokinen, NM Scheinin, S Aalto, K Någren, N Savisto, R Parkkola, J Rokka, M Haaparanta…
Parkinsonism & related disorders, 2010Elsevier
The objective of this study was to identify possible group differences between PD patients
with dementia and without dementia by combining different functional and structural imaging
methods in vivo, which might provide an opportunity to disentangle the pathophysiological
correlates of cognitive impairment and dementia in PD. We performed a neuropsychological
evaluation, structural brain MRI,[18F] FDG PET and [11C] PIB PET in 19 PD patients [eight
non-demented (PD), eleven demented (PDD)] and 24 healthy elderly volunteers.[11C] PIB …
The objective of this study was to identify possible group differences between PD patients with dementia and without dementia by combining different functional and structural imaging methods in vivo, which might provide an opportunity to disentangle the pathophysiological correlates of cognitive impairment and dementia in PD. We performed a neuropsychological evaluation, structural brain MRI, [18F]FDG PET and [11C]PIB PET in 19 PD patients [eight non-demented (PD), eleven demented (PDD)] and 24 healthy elderly volunteers. [11C]PIB region-to-cerebellum ratios did not differ significantly between the groups in any brain region (p > 0.05). PDD patients showed impaired glucose metabolism in cortical brain regions and this reduction was associated with the degree of cognitive impairment. PDD patients had more atrophy both in the hippocampus and the frontal cortex compared with PD patients and controls, and hippocampal atrophy was associated with impaired memory. This cross-sectional data suggests that development of dementia in PD is associated with extensive spread of hypometabolism beyond the occipital cortex, and with hippocampal and frontal atrophy but not beta-amyloid deposition consistent with a unique biological process related to PD rather than co-incidental development of AD in persons with PD.
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