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Amyloid imaging

The binding of the PET tracer N-methyl-11C-2-(4,-methylaminophenyl)-6-hydroxybenzothiazole (Pittsburgh Compound B, 11C-PIB) to fibrillary amyloid-beta provides an in vivo surrogate measure of the aggregation of amyloid protein. Increased binding of 11C-PIB relative to the cerebellum throughout the cortex has been found in AD [124], particularly in the posterior cingulate, frontal, lateral temporal, and parietal regions. Although increased uptake is a sensitive indicator of AD, 10-20% of subjects without any cognitive impairment also show increased 11C-PIB uptake [125, 126]. Studies of PD and PD-D generally demonstrate lower levels of cortical uptake when compared with AD patients and no significant increases in PD relative to controls; however, a subgroup of cases of PD-D may have increased uptake but to a lesser extent than that seen in DLB or AD [127-129].

Cardiac scintigraphy imaging

There is loss of sympathetic innervation in the heart in patients with PD [130]. This has been demonstrated with cardiac scintigraphy using 123I-metaiodobenzylguanidine ([123I]-MIBG), an analogue of noradrenaline, with the ratio of uptake in the heart to the mediastinum calculated to quantify the images. This ratio has been found to be reduced in PD and also in DLB and PD-D in comparison with both AD and healthy subjects [131]. Studies have found a diagnostic accuracy of approximately 90% for differentiating PD from other causes of neurodegenerative parkinsonism, with a sensitivity and specificity of 83% [132]. However, since decreased uptake is present in those with cardiovascular disease, caution must be exercised in the interpretation of MIBG scans in such patients [131].

Conclusion

Because the pathological, anatomical, and neurochemical mechanisms underlying the evolution of cognitive decline in PD are heterogeneous, it is unlikely that any single neuroimaging modality will be a reliable biomarker for all patients. Structural imaging studies with MRI have demonstrated that the evolution of dementia in PD is underpinned by significant and progressive loss of grey matter and disruption of the integrity of the white matter tracts. Functional imaging techniques show that such changes are accompanied by significant disturbances not only in perfusion and metabolism but also within the dopaminergic and cholinergic neurotransmitter systems, and these changes become more pronounced with disease progression.

Future research should focus on the development of harmonized protocols for image acquisition and processing to facilitate large multicentre studies, the development of radiotracers for a-synuclein and tau aggregation, and standardized neuropsychological testing schedules. Longitudinal studies should be of sufficient size and duration to track the significance of early cognitive changes and be able to correlate these to atrophic changes as they develop and include, where possible, pathological evaluation post-mortem.

 
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