Remember the Ice Bucket Challenge from 2014? The challenge, sponsored by the ALS Association, had people grabbing a bucket, filling it with ice and water and then dumping it on someone's head in order to promote awareness of amyotrophic lateral sclerosis (otherwise known as ALS or Lou Gehrig's Disease) and encourage donations for ALS research.
Well, as it turns out, the challenge did more than just "break the internet" - it actually worked. In an announcement on July 26, the ALS Association revealed that the 17 million people (including the likes of Bill Gates and Justin Bieber) who posted videos of themselves participating in the challenge have helped to raise enough money to fund an important research breakthrough.
So just how much money did the Ice Bucket Challenge raise? The ALS reports that $115 million was donated to the ALS Association, 67 percent of which went toward advancing research for treatments and a cure.
Thanks to some of that money ($1 million), researchers that were part of Project MinE, a University of Massachusetts Medical School Project, were able to identify a gene that is responsible for ALS, a rapidly progressive neurological illness that severely impacts the nerve cells that control the body's voluntary muscles. The condition causes the gradual deterioration of an individual's motor neurons, leading to their eventual demise.
The gene in question, NEK1, gives scientists another potential target for therapy development, bringing them once step closer to finding a way to treat the neurological disorder.
"The discovery of NEK1 highlights the value of 'big data' in ALS research," said researcher Lucie Bruijn. "The sophisticated gene analysis that led to this finding was only possible because of the large number of ALS samples available."
This is the third ALS-related gene researchers have discovered using money from the Ice Bucket Challenge. Last year, researchers at John Hopkins University looked at the role of a protein known as TDP-43 in the development of ALS. Throughout the study, they looked at how the protein broke down and became sticky, making it difficult for the team to analyze the DNA properly before the mice cells used died.
However, upon introducing a different kind of protein that was designed to replicate TDP-43 into the nerve cells, the mice cells returned to normal, suggesting that there is a treatment possible that could either slow down or prevent ALS from developing altogether.
In the meantime, the ALS Association notes that this discovery is quite special, since the project that found NEK1 is led by someone who suffers from ALS.
