{"id":4730,"date":"2021-03-11T20:13:46","date_gmt":"2021-03-12T01:13:46","guid":{"rendered":"https:\/\/ccna-ccnv.ca\/ccna_publication\/amyloid-s-impacts-future-freezing-of-gait-in-parkinsons-disease-via-white-matter-hyperintensities-2\/"},"modified":"2024-12-03T14:57:30","modified_gmt":"2024-12-03T19:57:30","slug":"amyloid-s-impacts-future-freezing-of-gait-in-parkinsons-disease-via-white-matter-hyperintensities-2","status":"publish","type":"ccna_publication","link":"https:\/\/ccna-ccnv.ca\/fr\/ccna_publication\/amyloid-s-impacts-future-freezing-of-gait-in-parkinsons-disease-via-white-matter-hyperintensities-2\/","title":{"rendered":"Amyloid \u00df Impacts Future Freezing of Gait in Parkinson\u2019s Disease Via White Matter Hyperintensities"},"content":{"rendered":"

Abstract<\/h2>\n
\n

Background<\/strong>\u00a0Freezing of gait (FOG) is a common symptom in Parkinson\u2019s Disease (PD) patients. Previous studies have reported relationships between FOG, substantia nigra (SN) degeneration, dopamine transporter (DAT) concentration, as well as amyloid \u03b2 deposition. However, there is a paucity of research on the concurrent impact of white matter damage.<\/p>\n<\/div>\n

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Objectives<\/strong>\u00a0To assess the inter-relationships between these different co-morbidities, their impact on future FOG and whether they act independently of each other.<\/p>\n<\/div>\n

\n

Methods<\/strong>\u00a0We used baseline MRI and longitudinal gait data from the Parkinson\u2019s 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 \u03b2 were obtained directly from the PPMI. Following correlation analyses, we investigated whether WMH burden mediates the impact of amyloid \u03b2 on future FOG.<\/p>\n<\/div>\n

\n

Results<\/strong>\u00a0SN DBM, WMH load, putamen and caudate DAT activity and CSF amyloid \u03b2 levels were significantly different between PD patients with and without future FOG (p < 0.008). Mediation analysis demonstrated an effect of CSF amyloid \u03b2 levels on future FOG via WMH load, independent of SN atrophy and striatal DAT activity levels.<\/p>\n<\/div>\n

\n

Conclusions<\/strong>\u00a0Amyloid \u03b2 might impact future FOG in PD patients through an increase in WMH burden, in a pathway independent of Lewy body pathology.<\/p>\n<\/div>\n","protected":false},"author":19,"featured_media":0,"template":"","meta":{"_acf_changed":false},"studies-relation":[],"class_list":["post-4730","ccna_publication","type-ccna_publication","status-publish","hentry"],"acf":[],"yoast_head":"\nAmyloid \u00df Impacts Future Freezing of Gait in Parkinson\u2019s Disease Via White Matter Hyperintensities - CCNA - CCNV<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/ccna-ccnv.ca\/fr\/ccna_publication\/amyloid-s-impacts-future-freezing-of-gait-in-parkinsons-disease-via-white-matter-hyperintensities-2\/\" \/>\n<meta property=\"og:locale\" content=\"fr_CA\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Amyloid \u00df Impacts Future Freezing of Gait in Parkinson\u2019s Disease Via White Matter Hyperintensities - 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