Funded Grants

In recent years, it was discovered that a microscopic worm called C. elegans could mimic some of the aspects of human ALS when they were engineered to have abnormal (mutant) genes that cause the disease.

In late 2011, a landmark discovery was made which identified that abnormalities (mutation) in a gene called C9ORF72 were responsible for the highest percentage of hereditary ALS and frontotemporal dementia cases.

ALS is a disease characterized by degeneration of both upper and lower motor neurons.

The blood-brain barrier (BBB) plays an essential role in protecting the brain from blood-borne diseases.

Toxic amyloid proteins are known to be a significant contributing factor in the development of Alzheimer’s disease.

In ALS, the disease is characterized by degeneration of motor neurons and an inability of the brain to signal the muscles to move, resulting in paralysis.

Discoveries made in Canada by the lab of Dr. Michael Strong over the past few years have implicated a protein called Rho guanidine nucleotide exchange factor (RGNEF) both pathologically and genetically in causing ALS.

Adolescence represents a unique developmental window of the life cycle to adopt healthy behaviours that will support psychosocial adjustment and well-being during adolescence and adulthood (World Health Organization, 2001).

Dr. Shmuel and his team are establishing a local platform which will support functional MRI (fMRI) in the alert non-human primate brain.

The Centre for Functional and Metabolic Mapping (CFMM) at Western’s Robarts Research Institute houses Canada’s only collection of high-field (3T human) and ultra-high field (7T human and 9.4T animal) MR systems.