Principal component analysis of PiB distribution in Parkinson and Alzheimer diseases

Campbell MC, Markham J, Flores H, Hartlein JM, Goate AM, Cairns NJ, Videen TO, Perlmutter JS; (2013) Neurology, 81 (6), pp. 520-527. Cited 1 time. Read More

Abstract

Objective: To use principal component analyses (PCA) of Pittsburgh compound B (PiB) PET imaging to determine whether the pattern of in vivo b-amyloid (Ab) in Parkinson disease (PD) with cognitive impairment is similar to the pattern found in symptomatic Alzheimer disease (AD). Methods: PiB PET scans were obtained from participants with PD with cognitive impairment (n 5 53), participants with symptomatic AD (n 5 35), and age-matched controls (n 5 67). All were assessed using the Clinical Dementia Rating and APOE genotype was determined in 137 participants. PCA was used to 1) determine the PiB binding pattern in AD, 2) determine a possible unique PD pattern, and 3) directly compare the PiB binding patterns in PD and AD groups. Results: The first 2 principal components (PC1 and PC2) significantly separated the AD and control participants (p < 0.001). Participants with PD with cognitive impairment also were significantly different from participants with symptomatic AD on both components (p < 0.001). However, there was no difference between PD and controls on either component. Even those participants with PD with elevated mean cortical binding potentials were significantly different from participants with AD on both components. Conclusion: Using PCA, we demonstrated that participants with PD with cognitive impairment do not exhibit the same PiB binding pattern as participants with AD. These data suggest that Ab deposition may play a different pathophysiologic role in the cognitive impairment of PD compared to that in AD.

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Posted on October 4, 2013
Posted in: HPAN, Neurogenetics, Publications Authors: , ,