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Weston Family Foundation awards two McGill researchers combatting neurodegenerative diseases of aging

Дата публикации: 22-01-2026 16:38:28




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Etienne de Villers-Sidani and Philippe Huot have been awarded funding from the Weston Family Foundation’s Rapid Response program for their innovative research advancing diagnostic tools and interventions for Alzheimer's disease and Parkinson’s disease. They are among seven researchers nationwide to receive funding in this year’s competition, announced this week.

The Weston Family Foundation, through the Weston Brain Institute and the Weston Family Microbiome Initiative, supports science-based approaches to significantly improve the health and well-being of Canadians. The Rapid Response program funds high-risk, high-reward translational research that accelerates the development of therapeutics or tools for neurodegenerative diseases of aging. 
 
Etienne de Villers-Sidani, Associate Professor in the Department of Neurology and Neurosurgery, received funding for his project titled “Development and validation of a digital biomarker-based tool for the early screening and monitoring of Alzheimer’s Disease”. 
 
Professor De Villers-Sidani will validate a novel mobile tool for monitoring Alzheimer’s disease using a multi-site, multi-phase cross-sectional study with multiple cohorts of AD patients. The Eye-Tracking Neurological Assessment for Alzheimer’s Disease (ETNA™-AD) uses an iPad’s embedded camera to analyze eye movements, which can inform on the presence of neurodegeneration and cognitive impairment. The device has the potential to offer a fast, non-invasive, and scalable alternative to lengthy clinical assessments.  

Phillipe Huot, Associate Professor in the Department of Neurology & Neurosurgery, received funding for his project titled “Characterisation of novel GlyT1 inhibitors for the treatment of Parkinson’s disease”.   

Professor Huot and his team will study a novel therapeutic strategy aimed at improving the effectiveness of Parkinson’s disease treatments while reducing their most debilitating side effects. His team has demonstrated that inhibiting the glycine transporter 1 (GlyT1) can both enhance the anti-parkinsonian effects of L-DOPA, the current gold-standard therapy, and significantly reduce L-DOPA-induced dyskinesia—involuntary, abnormal movements often occurring with long-term use of medications for Parkinson's—a major limitation of long-term treatment. Unlike existing therapies, GlyT1 inhibitors may also reduce psychosis-like behaviours without exacerbating motor complications. Building on these findings, Professor Huot and his team will assess novel GlyT1 inhibitor compounds optimized for improved efficacy and safety. They will now characterize candidates using rodent models to advance a potentially new best-in-class, differentiated therapy. 

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