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The overall goal of this research program is to identify genomic markers that predict small vessel disease of the brain.

When cells are under stress, one of the reactions is to form tiny clumps called stress granules that protect important genetic information while protective mechanisms kick in.

The four most commonly studied ALS proteins are SOD1, TDP-43, FUS and C9ORF72

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.