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Amyloid beta and white matter hyperintensities collude to freeze gait in Parkinson’s disease

Updated: Mar 11, 2021


This upcoming Saturday 13 March at 9h30 (Eastern Std Time), Mahsa (Dadar) will be presenting her work titled ”WHITE MATTER HYPERINTENSITIES, AMYLOID BETA, LEWY BODY PATHOLOGY, AND FUTURE FREEZING OF GAIT IN PARKINSON’S DISEASEat the 2021 AD/PD Conference.


This work was done as part of her current post-doctoral studies, which she does under the joint supervision of Richard (Camicioli), from U. of Alberta, and our lab. She wanted to analyze what were the biomarkers of interest that were related to Freezing of Gait (FOG) in Parkinson‘s disease (PD).

FOG is a sudden, transient and unexpected interruption in walking, usually during gait initiation or while turning. It is one of the major motor dysfunctions that manifest in PD patients - up to 25% of them. As one can surmise, FOG will increase the risk of falls and injury, and impacts the quality of life for these individuals, particularly in the later stages of the disease.

At present, FOG poses an unmet need as neither medications nor advanced therapies such as deep brain stimulation reliably and significantly improve FOG outcomes. Part of the reason for this lack of efficient therapies is that we lack a clear understanding of the determinants of future FOG.

Part of the story might be related to a culprit that is well-known to Alzheimer’s disease researchers, namely amyloid beta (Aβ) - which also occurs in individuals with PD.

Mahsa wanted to ask if Aβ, together or independently of white matter hyperintensities, a marker of cerebrovascular lesions, impact FOG. To answer this question, she studied data collected from participants in the Parkinson’s Progression Markers Initiative using a variety of techniques - deformation based morphometry, cerebrospinal fluid biomarkers, WMH lesion segmentations - together with statistical analysis,

What she found through mediation analysis was that Aβ impacts future FOG through an increase in WMH burden, independently of substantia nigra atrophy, striatal dopamine activity, age, sex, disease duration, Levodopa equivalent dose, or the use of cardiovascular medication.

Taken together, her results suggest that development of FOG in de novo PD patients has a multi-pathway etiology, emphasizing the need for multi-modal therapeutic interventions in PD, including those targeting cerebrovascular risk factors.

Once again, please tune in to the AD/PD conference to watch her provide more information on this topic.



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