By Andy Choi
Parkinson’s disease dementia (PDD) develops through the evolution of the Lewy body pathology responsible for PD with simultaneous Parkinson’s disease Alzheimer’s disease (PDAD).
A research team conducted several experiments on patients and observed that amyloid plaques were more accumulated in the striatal area of the brain of PDAD patients than in PDD patients. Using advanced imaging techniques, the striatal amyloid plaques that occur in the living brain can be detected, through which PDD could also be differentiated from PDAD.
The research findings have been released in the Journal of Parkinson’s Disease.
Several aged patients volunteered for the Arizona Parkinson’s disease Consortium and Banner Sun Health Research Institute Brain and Body Donation Program. Autopsies were conducted on the brains of these patients. The program involved a longitudinal clinicopathological study on Parkinsonism, normal aging, and dementia. Evaluation was performed with brain, which included a diagnosis of PDAD, PDD without pathological AD, and PD without dementia (PDND). In addition, comparative studies were carried out with former observations on patients with AD without PD (AD), which also included non-demented normal control patients without parkinsonism (NC). Researchers graded amyloid plaque densities within the brain as sparse, none, frequent or moderate. The overall plaque score featured diffuse, cored, and neuritic. Separate scores were obtained with cored and neuritic plaques.
When compared to PDD, PDND, and NC patients, researchers determined that the neuritic plaque density and cerebral cortex total scores were higher for AD and PDAD cases. The PD patients with any type of striatal plaques indicated clinicopathological diagnosis of AD with 80% specificity and sensitivity. Regarding PDND, PDAD, and PDD, the presence of cerebral cortex plaques showed 100% sensitivity and were 48% specific. PDAD and PDD groups were 55% specific.