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The rs6971 TSPO polymorphism does not influence disease presentation or progression in Parkinson's disease

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Peer-reviewed

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Abstract

Mitochondrial translocator protein (TPSO) PET imaging is widely used to study neuroinflammation in vivo. TSPO, located on the outer mitochondrial membrane, is upregulated in microglia in association with neuroinflammation1, with increased binding observed in Parkinson’s disease (PD)2. The first-generation TSPO ligand [11C]PK11195 has important limitations due to low signal-to-noise ratio, and a high production failure rate. Second generation TSPO ligands (e.g. [11C]PBR28 /[18F]DPA714) offer improved binding affinity, specificity and bioavailability3, making them valuable in clinical studies as an index of brain inflammation. Since chronic neuroinflammation emerges early in PD and potentially drives disease progression4, TSPO-PET imaging can help evaluate the effectiveness of anti-inflammatory therapies and support the development of disease-modifying therapies.

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Movement Disorders

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Journal ISSN

0885-3185
1531-8257

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Wiley

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Except where otherwised noted, this item's license is described as Attribution 4.0 International
Sponsorship
This work was supported by the NIHR Cambridge Biomedical Research Centre (NIHR203312). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. The CamPaIGN study has received funding from the Wellcome Trust, the Medical Research Council, and the Patrick Berthoud Trust. The PICNICS study has received funding from the Cure Parkinson’s Trust, the Van Geest Foundation, the Medical Research Council and Parkinson’s UK. CHWG was supported by a RCUK/UKRI Research Innovation Fellowship awarded by the Medical Research Council (MR/R007446/1; MR/W029235/1) and received support from the Cambridge Centre for Parkinson-Plus. The authors declare there are no conflicts of interest to report.