Climbs atop soapbox-
It's easy to be cynical about social media exploits, and surely many people doing this are just doing it as a stunt to be part of the party. However, even if they are just perpetuating the stunt so it can reach someone else who will care to learn, and to donate then they are serving a useful purpose here. Also, yes you would hope that people express some dignity or respect for the people and families who suffer from the disease, but then we all fall short of showing proper consideration for others from time to time.
In any event this "challenge", "stunt", "Social-media hullabaloo" whatever you call it has raised a crap ton of money for a rare disease foundation. My primary research project is on a rare disease (not ALS), and I can tell you first hand that these patient/disease advocacy foundations can serve a role that no other existing public or private groups can. They have the ability to draw together patient groups, basic scientists (read academics), contract commercial research organizations and drug developers (read biotechs and pharma) in a way that really does drive understanding of and ultimately progress on these diseases. ALS is a particularly hard disease because we only know what causes a small percentage of the cases (protein misfolding of SOD1), and it's real hard and expensive to try to figure out how to treat a disease when you don't know what causes it, theories are damn expensive to test...look at the tens of billions of dollars and hundreds of thousands of man years of effort (neither number is an exaggeration, in fact Alzheimer's is probably into the millions of man years of effort at this point) spent on attempted treatment of Alzheimer's as a for instance. Even the cases of ALS we do know the cause of (toxic gain of function misfold of SOD1) are caused by about the most complex root of disease to treat. There is only one drug I know of (VX-809 for Cystic Fibrosis) that has demonstrated an ability to aid in a misfolded protein disease by interacting with the protein itself to influence its folding directly (probably the mode of action), not just mucking up the folding and quality control machinery (read as big time side effects and often incompatible with life). CF is even an easier situation because it is a loss of function mutation, not a toxic gain of function mutation. Incidentally, you need SOD1 or your brain will basically oxidize itself to death, so no just getting rid of it (which would itself be challenging also).
To summarize, if you donated to this cause you donated to a good cause. If you dumped ice on yourself, didn't donate, acted like a fool, called out someone who may give a damn, then I am also glad you did it (though I reserve the right to :eyeroll
. In the end I don't care why you did it, I'm a pragmatist I guess. ALS is a scientific problem so immense that it is only going to be solved by throwing money and effort (funded by money, I know few independently wealth scientists) at good ideas, of which the overwhelming majority will be wrong, but only one needs to work. Also, what is learned in the effort (successes and failures) about the fundamentals of protein folding diseases and neuro-muscular diseases will benefit research into Huntington's, CF, certain Mitochondrial diseases, possibly Alzheimer's, and myriad others I'm sure.
-Steps off soapbox, waits for flying tomatoes
