Isolated cognitive impairments and dementia are common in Parkinson’s disease (PD). In this study, we evaluated
the extent of Aβ accumulation in non-demented PD individuals and the relation of global and regional Aβ to
35 non-demented PD subjects underwent neurological examination, cognitive testing, and PiB PET. To assess
regional amyloid burden, 20 subjects also underwent high resolution MRI for Freesurfer processing and
partial volume correction. 16 cortical ROIs that are associated with high amyloid deposition in Alzheimer’s
disease were selected for analysis. PiB DVR values in ROI were left-right averaged. The 35 PD subjects
(men/women = 26/9) had a mean age of 69 years, education of 16.5 years and Hoehn & Yahr stage of 2.3; the
mean MMSE was 28.
Global, non-partial volume corrected PiB DVR (with cerebellar reference) ranged from 0.98 to 1.57
(mean±SD: 1.18±0.14), and did not differentiate those with (n=15) and without (n=20) specific cognitive impairments
(defined as CDR-sum of boxes score [CDR-SOB]>0). Across 11/16 ROIs, partial volume corrected regional
amyloid burden correlated with increased impairment on CDR-SOB (p<0.04 for each correlation, covarying
for age). A multiple regression analysis revealed a linear combination of 5 ROIs that significantly predicted the
CDR-SOB (p<0.0001). In addition, amyloid deposition in medial temporal lobe structures (the hippocampus,
parahippocampus, and entorhinal cortex), significantly correlated with short term memory impairment (logical
memory IIa and the free recall component of the selective reminding test, covarying for age). When three subjects
with PD dementia were included in this analysis, these correlations grew stronger and PiB DVR in the anterior
cingulate also correlated significantly with memory impairment.
These results suggest that Aβ-amyloid accumulation is a frequent finding in non-demented PD patients and that
regional amyloid burden relates to cognitive performance in PD, supporting the possibility that Aβ may be a risk
factor in PD for developing dementia.
This research is supported by the Michael J Fox PD Foundation.