Here’s the Exact Way That the Ice Bucket Challenge Helped ALS Research

Last twelvemonth ’s hugely popular “ ice pail challenge ” realize celebrities pouring bucket of chicken feed water over their heads to help agitate Lou Gehrig ’s Disease ( ALS).Skepticsdismissed it as mere “ slacktivism , ” but researchers told us that the money led directly to a scientific find . Can slacktivism actually work ?

Earlier this month , Nicholas Kristof wrote a rathergloating Op - Edin the New York Times , chafing at the critique that such effort are mostly ineffective and nonmeaningful . After all , some 17 million people participated in the challenge , andthe ALS Association claimsit raised $ 115 million in six week for the cause . Money does n’t mean scientific find follow , however .

But in former August , researcher at Johns Hopkins University announced apotential breakthrough therapy for ALS . JHU ’s Philip Wong’stold the pressthat “ The financial support [ from the ice bucketful challenge ] certainly help the solvent we obtained . ” That seemed to support Kristof ’s claim , but could it really be that mere ? We wanted to roll in the hay more .

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First , justwhat is this big breakthroughthatappeared in the daybook Science ? It centre on a particular protein , TDP-43 , that is recognize to make clumps inside the learning ability cubicle of almost all people with ALS ( 97 % ) , as well as in 45 % of those support from dementia . But the precise role of this protein , or just what effects that clumping had , were n’t have it away .

The JHU investigator figured out that in healthy citizenry , TDP-43 protects cells by ensuring that wrong RNA segment are n’t include in the “ blueprint ” for manufacturing other protein . ( As Francis Crick sententiously keep : “ desoxyribonucleic acid make RNA , RNA make proteins , and protein make us . ” ) But when those clumps form , the TDP-43 no longer functions properly . It ’s as if the protein is n’t present at all and the cells ca n’t read the “ design . ” And without that aegis , those mastermind cellular telephone start to go bad .

The JHU team even manage to save dying jail cell by plugging in a different , custom - designed protein to mimic the function of the defective TDP-43 . And it worked ! The damaged electric cell returned to normal . “ We can for the very first time make these zombie - like cellular telephone where they do n’t have any TDP-43 but they subsist , ” lead author Jonathan Ling told Gizmodo . “ No one has ever shown that . ” So there is now a path forwards toward developing an effective gene therapy to combat ALS .

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This is very exciting poppycock . But can we really maneuver to a direct crusade - and - effect link between this new solvent and the funds raise by the ice bucket challenge ? The result is a bit more nuanced than that .

Breakthroughs do n’t materialise in a vacuity , despite what the headlines would have you believe . There are months , year , sometimes decades of toiling in reconditeness before that big eureka ! present moment arrives . JHU ’s research syllabus on TDP-43 was already well afoot before the lab received extra funding from the Methedrine bucket challenge . It was the timing of the funds that seems to have made the difference , fit in to Wong ’s statements to the press .

Ling confirmed to Gizmodo that the challenge - related grant the science laboratory received from the Robert Packard Center for ALS Research “ was a big assist towards the end of the study . It was good to have that money come in at that meter . ” ( They also incur additional challenge - bear on funds from the ALS Association after the report was everlasting . ) They had collected enough datum to warrant a journal reassessment outgrowth for their draft paper , but that takes several months . And reviewers inevitably want more experiments to be done before green - ignition a paper for publication , which takes money . [ Note 9/18/15 : This paragraph has been updated to clarify which challenge - related store came from which organization . ]

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Ling acknowledged that they might have managed to pull a few string and get more funding without the challenge , but there was no warrant of success , especially since plenty of scientists were skeptical about their hypothesis . So much prior piece of work had been done on this particular protein ; sure as shooting if there was anything significant there , the reasoning went , someone else would have found it by now . “ This is the job with science , ” said Ling . “ Once people get set in their thinking , the onus is on you ” to turn out otherwise .

The engineering science used in this special experiment is call RNA - seq ( sequence ) , which hotfoot up the process of sequencing genetic entropy . But it is also ridiculously expensive — and it still take several month to march samples because there are foresighted wait lists to utilize these rarefied multimillion dollar bill machines . “ It ’s a vast risk of infection to put all of your eggs into one basket , ” Ling said . “ If you examine to engage in a high-pitched risk , high reinforcement experimentation , and it does n’t end up working , then you ’re out of money to do the body of work you ’re supposed to do . ”

So the ALS investment company might not have led at once to this new therapeutical strategy , but that money accelerated the lab ’s progress by allow them to do a dear experimentation that they might otherwise not have been able to yield . Ling estimates it would have taken another two to three years at least without it . That ’s not very recollective in the world of scientific research , but it is an eternity to someone put up from ALS , which kills most patients within two to five years . So in that mother wit , we can call the ice bucket take exception a success .

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Exciting though this experimental result may be , it is not a sorcerous “ cure ” for ALS — or even a fully develop therapy . The pivotal experiment was done on science laboratory - grown cell , not whole living being . The next step for the JHU radical is to test their designer protein that mimics TDP-43 on shiner . If that run , it must then be tested on humans . The good intelligence is that TDP-43 mapping the same in both mice and humans — indeed , in middling much every high - order being , according to Ling . It just does its thing in unlike location .

“ Just because you see it in 97 % of patients , we still do n’t screw whether it ’s have the disease or if it ’s merely a symptom of the disease , ” Ling said . “ What we do know is that if you remove [ TDP-43 ] from a neuron , that neuron will die . We may just be slow up thing down . ” The only way to know for sure is to conduct a clinical tryout . Andclinical trial are expensive .

Hmmm . It might be time to break out the ice buckets again .

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