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One of the hallmarks of ALS is the presence of abnormal clumps inside motor neurons that contain various substances which include, in the majority of cases, something called TAR DNA–binding protein 43 (TDP-43).

In some cases of ALS, it is clear that specific inherited genetic changes (called mutations) can not only cause the disease, but can do so by creating a protein (the end product of genes that actually does a function in our cells) that has an abnormal, toxic function resulting in motor neuron degeneration.

It has been more than a decade since scientists proved that ALS is not simply a disease of motor neurons, but that other cells in the neighbourhood around them could play an active role in the disease process.

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.