ArticleClinical and translational imaging2015
Imaging Amyloidopathy in Parkinson Disease and Parkinsonian Dementia Syndromes.
Article in Clinical and translational imaging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed.
- Serum Aberrant Expression of miR-431-5p and Their Diagnostic Value in Parkinson's Disease.Neurochemical research · 2026Article
- Apathy linked to higher amyloid burden and cognitive deterioration in Parkinson's disease.Journal of Parkinson's disease · 2025Observational
- Neuroimaging and fluid biomarkers in Parkinson's disease in an era of targeted interventions.Nature communications · 2024Review
- Pathobiology of Cognitive Impairment in Parkinson Disease: Challenges and Outlooks.International journal of molecular sciences · 2023Review
- Morphological basis of Parkinson disease-associated cognitive impairment: an update.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Acetylcholinesterase Inhibitors in the Treatment of Neurodegenerative Diseases and the Role of Acetylcholinesterase in their Pathogenesis.International journal of molecular sciences · 2021Review
- Apathy rating scores and β-amyloidopathy in patients with Parkinson disease at risk for cognitive decline.Neurology · 2020Article
- Network connectivity determines cortical thinning in early Parkinson's disease progression.Nature communications · 2018Article
- Molecular Imaging and Updated Diagnostic Criteria in Lewy Body Dementias.Current neurology and neuroscience reports · 2017Review
- Striatal and Cortical β-Amyloidopathy and Cognition in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2016Article
- Cognitive Profile in Parkinson's Disease Dementia Patients with Low versus Normal Cerebrospinal Fluid Amyloid Beta.Dementia and geriatric cognitive disorders extraArticle
- Magnetic resonance imaging and positron emission tomography in the diagnosis of neurodegenerative dementias.Functional neurologyReview
Corrections and comments
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Authors and funding
2 authors.
Funding
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 one 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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Registered trials
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