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Imaging amyloidopathy in Parkinson disease and parkinsonian dementia syndromes

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Abstract

Dementia arising in patients with Parkinson disease or parkinsonian neurodegeneration comprises a heterogeneous neuropathology. Clinical labeling of patients with both dementia and Parkinson disease is dichotomous, depending on the temporal development of cognitive impairment and motor parkinsonism. Patients with dementia arising first (or within the first year of PD) are classified as dementia with Lewy bodies; patients with PD for more than 1 year before cognitive decline are classified as Parkinson disease with dementia. Despite this differential clinical classification, autopsy studies demonstrate variable admixtures of cortical synuicleinopathy, Aβ-amyloidopathy and tau neurofibrillary tangle deposition. There are no routine clinical diagnostic measures that accurately distinguish the underlying neuropathologies in individual patients. In the present paper, we review the published literature describing characteristics of fibrillary Aβ-amyloid deposition on the basis of PET radiotracer imaging in patients with Parkinson disease and in parkinsonian dementia syndromes. Although individual reports often include only small-to-modest subject numbers, there is overall suggestion that PD patients have a lower incidence of Aβ-amyloid deposition than seen amongst elderly normal subjects, and that Parkinson disease with dementia patients have a lower incidence of Aβ-amyloid deposition than do patients with dementia with Lewy bodies. These apparent features contrast the findings of Aβ-amyloid-PET imaging in normal aging and the development of Alzheimer disease, where Aβ-amyloid deposition arises asymptomatically and apparently many years before development of signs or symptoms of dementia. It is proposed that focused, prospective studies are needed to further address and understand the complex role(s) of Aβ-amyloid pathology in Parkinson disease, and that this understanding will be critical to the development of targeted disease-modifying therapy for dementia in PD.

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Conflict of interest

Dr. Frey lists grant support from General Electric and consulting activities with Siemens, Avid Radiopharmaceuticals and MIM Software. He holds general stock interests in Bristol Myers Squibb, Medtronic, Merck and Novo-Nordisk. Dr. Petrou lists no potential conflicts.

Compliance with ethical standard

No direct participation of human or experimental animal subjects was involved in this reporting; all data discussed and presented are derived from previously published scientific reports.

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Authors and Affiliations

  1. Departments of Radiology and Neurology and the Molecular and Behavioral Neuroscience Institute, The University of Michigan, Ann Arbor, MI, USA

    Kirk A. Frey

  2. Division of Nuclear Medicine, The University of Michigan, 1500 East Medical Center Drive, Room B1G-505 UH, Ann Arbor, MI, 48109-5028, USA

    Kirk A. Frey

  3. Department of Radiology, The University of Michigan, Ann Arbor, MI, USA

    Myria Petrou

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Frey, K.A., Petrou, M. Imaging amyloidopathy in Parkinson disease and parkinsonian dementia syndromes. Clin Transl Imaging 3, 57–64 (2015). https://doi.org/10.1007/s40336-015-0104-4

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