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    Reduced striatal vesicular monoamine transporter 2 in REM sleep behavior disorder: imaging prodromal parkinsonism

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    Author
    Beauchamp, LC; Villemagne, VL; Finkelstein, D; Dore, V; Bush, A; Barnham, KJ; Rowe, CC
    Date
    2020-10-23
    Source Title
    Scientific Reports
    Publisher
    NATURE RESEARCH
    University of Melbourne Author/s
    Bush, Ashley; Finkelstein, David; Barnham, Kevin; Rowe, Christopher; Beauchamp, Leah
    Affiliation
    Florey Department of Neuroscience and Mental Health
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Beauchamp, L. C., Villemagne, V. L., Finkelstein, D., Dore, V., Bush, A., Barnham, K. J. & Rowe, C. C. (2020). Reduced striatal vesicular monoamine transporter 2 in REM sleep behavior disorder: imaging prodromal parkinsonism. SCIENTIFIC REPORTS, 10 (1), https://doi.org/10.1038/s41598-020-74495-x.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/251747
    DOI
    10.1038/s41598-020-74495-x
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7584593
    Abstract
    Motor deficits in parkinsonism are caused by degeneration of dopaminergic nigral neurons. The success of disease-modifying therapies relies on early detection of the underlying pathological process, leading to early interventions in the disease phenotype. Healthy (n = 16), REM sleep behavior disorder (RBD) (n = 14), dementia with Lewy bodies (n = 10), and Parkinson's disease (PD) (n = 20) participants underwent 18F-AV133 vesicular monoamine transporter type-2 (VMAT2) PET to determine the integrity of the nigrostriatal pathway. Clinical, neurophysiological and neuropsychological testing was conducted to assess parkinsonian symptoms. There was reduced VMAT2 levels in RBD participants in the caudate and putamen, indicating nigrostriatal degeneration. RBD patients also presented with hyposmia and anxiety, non-motor symptoms associated with parkinsonism. 18F-AV133 VMAT2 PET allows identification of underlying nigrostriatal degeneration in RBD patients. These findings align with observations of concurrent non-motor symptoms in PD and RBD participants of the Parkinson's Progression Markers Initiative. Together, these findings suggest that RBD subjects have prodromal parkinsonism supporting the concept of conducting neuroprotective therapeutic trials in RBD-enriched cohorts. Ongoing longitudinal follow-up of these subjects will allow us to determine the time-window of clinical progression.

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