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Leading the Fight to treat and cure
Tay-Sachs, Canavan, Sandhoff, GM1 and related diseases

Brennan the Brave

Brennan Stringer was born July 21, 2012.

He was born seemingly healthy, clocking in at 8 lbs. 11 oz. As most babies, Brennan had his little quirks like acid reflux but nothing out of the ordinary. It wasn't until about 6 months of age that we started to notice a difference in Brennan's development. He had quickly learned how to sit up, but came to a screeching halt after that. And as we would watch the next 6 months unfold, his development would drastically decline.

On September 24th, 2013, at 14 months of age, Brennan was diagnosed with Infantile Tay-Sachs Disease. Our neurologist explained that such disease has been terminal in all children, with most children not living past the age of four. There is currently no cure and little treatment. We were glad to finally have an answer, but devastated by the diagnosis.

Brennan, whose name means "Brave", went from being a seemingly healthy little boy, sitting up and saying "Mamma," to being completely immobile and suffering from a life-threatening disease in only a matter of a few months.

Words cannot express what a privilege it was to be Brennan's parents. The Lord chose us to care for this precious child and now he is home. Brennan passed on March 4, 2016, in the comfort of his own home. 

- Holly and Royce Stringer (Brennan's parents)

What is Tay-Sachs?

Tay-Sachs disease is caused by the absence or significantly reduced level of a vital enzyme called beta-hexosaminidase. It is the Hexosaminidase A (HEXA) gene in the DNA that provides instructions for making this enzyme. Without the correct amount of the HexA enzyme, a fatty substance or lipid called GM2 ganglioside accumulates abnormally in cells, especially in the nerve cells of the brain. This ongoing accumulation, also called "substrate", causes progressive damage to the cells.

Infantile Tay-Sachs is typically the absence of the HexA enzyme. This differs from the Juvenile and Late Onset forms of Tay-Sachs when the mutations allow the HexA enzyme to function a little bit. Just a small increase in HexA activity is enough to delay the onset and slow the progression of symptoms.

What about research?

Tay-Sachs Disease research is usually performed simultaneously with Sandhoff disease research. This is because these two diseases have a similar underlying biochemical mechanism.

Read more about the Research We Fund here.

Read past NTSAD's Research Reviews here.

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