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Amyloid ß Impacts Future Freezing of Gait in Parkinson’s Disease Via White Matter Hyperintensities

Mahsa Dadar, Janis Miyasaki, Simon Duchesne, Richard Camicioli
doi: https://doi.org/10.1101/2020.10.29.360552
Mahsa Dadar
1CERVO Brain Research Center, Centre intégré universitaire santé et services sociaux de la Capitale Nationale, Québec, QC
PhD
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  • For correspondence: mahsa.dadar.1@ulaval.ca
Janis Miyasaki
3Neuroscience and Mental Health Institute and Department of Medicine, Division of Neurology, University of Alberta, Edmonton, AB
MD
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Simon Duchesne
1CERVO Brain Research Center, Centre intégré universitaire santé et services sociaux de la Capitale Nationale, Québec, QC
2Department of Radiology and Nuclear Medicine, Faculty of Medicine, Université Laval, Québec, QC
PhD
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Richard Camicioli
3Neuroscience and Mental Health Institute and Department of Medicine, Division of Neurology, University of Alberta, Edmonton, AB
MD
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Abstract

Background Freezing of gait (FOG) is a common symptom in Parkinson’s Disease (PD) patients. Previous studies have reported relationships between FOG, substantia nigra (SN) degeneration, dopamine transporter (DAT) concentration, as well as amyloid β deposition. However, there is a paucity of research on the concurrent impact of white matter damage.

Objectives To assess the inter-relationships between these different co-morbidities, their impact on future FOG and whether they act independently of each other.

Methods We used baseline MRI and longitudinal gait data from the Parkinson’s Progression Markers Initiative (PPMI). We used deformation based morphometry (DBM) from T1-weighted MRI to measure SN atrophy, and segmentation of white matter hyperintensities (WMH) as a measure of WM pathological load. Putamen and caudate DAT levels from SPECT as well as cerebrospinal fluid (CSF) amyloid β were obtained directly from the PPMI. Following correlation analyses, we investigated whether WMH burden mediates the impact of amyloid β on future FOG.

Results SN DBM, WMH load, putamen and caudate DAT activity and CSF amyloid β levels were significantly different between PD patients with and without future FOG (p < 0.008). Mediation analysis demonstrated an effect of CSF amyloid β levels on future FOG via WMH load, independent of SN atrophy and striatal DAT activity levels.

Conclusions Amyloid β might impact future FOG in PD patients through an increase in WMH burden, in a pathway independent of Lewy body pathology.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted October 29, 2020.
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Amyloid ß Impacts Future Freezing of Gait in Parkinson’s Disease Via White Matter Hyperintensities
Mahsa Dadar, Janis Miyasaki, Simon Duchesne, Richard Camicioli
bioRxiv 2020.10.29.360552; doi: https://doi.org/10.1101/2020.10.29.360552
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Amyloid ß Impacts Future Freezing of Gait in Parkinson’s Disease Via White Matter Hyperintensities
Mahsa Dadar, Janis Miyasaki, Simon Duchesne, Richard Camicioli
bioRxiv 2020.10.29.360552; doi: https://doi.org/10.1101/2020.10.29.360552

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