Alterations in Purkinje cell synaptic terminals in the CN are among the first changes observed in ARSACS mice. Given the prevalent hypothesis that presynaptic changes lead to eventual cell death of the parent cell, we believe that understanding this is likely to provide novel therapeutic targets to prevent Purkinje cell loss. Our current results point to the interplay of neuronal synapses and the pro inflammatory milieu of astrocytes and microglia as players in the CN dysfunction. By identifying early synaptic and neuroinflammatory mechanisms that drive Purkinje cell degeneration, this work may reveal novel disease-modifying therapeutic targets for ARSACS. Although still in relatively early preclinical stages, these studies could establish future translational strategies aimed at slowing neurodegeneration and preserving motor function in patients.
Subvention : $100 000
Durée : un an
Dr. Alanna Watt
Professor, Department of Biology
Dean, Faculty of Science
McGill University
Bellini Life Sciences Complex
3649 Sir William Osler
Montreal, Quebec H3G 0B1
Contact : alanna.watt@mcgill.ca