A group of researchers in Ireland has retracted their 2013 article on a possible new method for treating amyotrophic lateral sclerosis — ALS, also commonly called Lou Gehrig’s disease — after identifying errors in several images in the paper.
The article, “Acidotoxicity and acid-sensing ion channels contribute to motoneuron degeneration,” was published online in Cell Death & Differentiation (and appeared in the April 1 print issue, although we think that was a coincidence…).
According to the abstract:
Amyotrophic lateral sclerosis (ALS) is a fatal neurological condition with no cure. Mitochondrial dysfunction, Ca2|[plus]| overloading and local hypoxic|[sol]|ischemic environments have been implicated in the pathophysiology of ALS and are conditions that may initiate metabolic acidosis in the affected tissue. We tested the hypothesis that acidotoxicity and acid-sensing ion channels (ASICs) are involved in the pathophysiology of ALS. We found that motoneurons were selectively vulnerable to acidotoxicity in vitro, and that acidotoxicity was partially reduced in asic1a-deficient motoneuron cultures. Cross-breeding of SOD1G93A ALS mice with asic1a-deficient mice delayed the onset and progression of motor dysfunction in SOD1 mice. Interestingly, we also noted a strong increase in ASIC2 expression in motoneurons of SOD1 mice and sporadic ALS patients during disease progression. Pharmacological pan-inhibition of ASIC channels with the lipophilic amiloride derivative, 5-(N,N-dimethyl)-amiloride hydrochloride, potently protected cultured motoneurons against acidotoxicity, and, given post-symptom onset, significantly improved lifespan, motor performance and motoneuron survival in SOD1 mice. Together, our data provide strong evidence for the involvement of acidotoxicity and ASIC channels in motoneuron degeneration, and highlight the potential of ASIC inhibitors as a new treatment approach for ALS.
So much for that strong evidence. As the retraction notice states:
The authors wish to retract the above paper. The journal has recently been notified by a reader who expressed concerns about some of the figures in this paper. Dr. Áine Behan, co-investigator of this study, has acknowledged sole responsibility for errors affecting certain panels in Figures 2b and 5, in which data were processed with the result that the figure panels do not correctly reflect the original data. Dr. Behan and co-author Dr. Bridget Breen have acknowledged responsibility for clerical errors in Figures 8b and 2a, respectively. Dr. Behan and Dr. Breen regret these errors, of which the co-authors Marion Hogg, Ina Woods, Karen Coughlan, Mollie Mitchem and Jochen Prehn were completely unaware. We thank the reader for bringing this to our attention and sincerely apologize to the scientific community for any confusion or adverse consequences resulting from the publication of these data.
Of course, what “clerical errors” might mean is anyone’s guess. But the explanation for the flaws in figures 2b and 5 is, well, risible. How is saying that the “data were processed with the result that the figure panels do not correctly reflect the original data” different from saying “I falsified it?”
The paper has been cited three times, according to Thomson Scientific’s Web of Knowledge.
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