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The first genetic cause of ALS to be discovered (in 1993) encoded a mutation in protein called superoxide dismutase 1 (SOD1).

Tissue engineering is a process that was originally designed and continues to be used for growing cells outside the body, turning them into functional tissues and organs, and applying them for clinical use.

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.

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.

Earlier diagnosis of ALS remains one of the biggest goals of researchers worldwide and it is likely that the effectiveness of future treatment discoveries will be magnified by their application at a time point closer to symptom onset.

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

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.

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.

This project will use cells found in bone marrow as a potential means of delivering treatments to the diseased area in brain and spinal cord.

Motor neurons are made up of three distinct regions. The top of the neuron is composed of branches like a tree called dendrites that receive information to transmit.