Ágnes Patzkó, Yunhong Bai, Mario A. Saporta, István Katona, XingYao Wu, Domenica Vizzuso, M. Laura Feltri, Suola Wang, Lisa M. Dillon, John Kamholz, Daniel Kirschner, Fazlul H. Sarkar, Lawrence Wrabetz and Michael E. Shy. Curcumin derivatives promote Schwann cell differentiation and improve neuropathy in R98C CMT1B mice. Brain 2012;135:; doi:10.1093/brain/aws299.
The authors would like to apologize for an error in Fig. 2A in the above manuscript. The images from the wild-type untreated mouse and the wild-type mouse treated with CO were inadvertently both taken from the same untreated animal. We now supply a corrected version of the figure in which the wild-type images are from the correctly labelled animals. We are embarrassed by our error. It has no bearing on the interpretation of the figure, which was that neither PCC nor CO had any direct effect on myelination of wild type or mutant animals.
PCC or CO treatment does not affect myelination directly, but exerts its effects on axons. (A) Semi-thin sections illustrate hypomyelination and the absence of large diameter fibres in R98C/+ animals, and severe dysmyelination in R98C/R98C mice. Several large diameter fibres can be observed in PCC or CO treated R98C/+ animals. Treatment failed to improve hypomyelination. Bar =10 μm. (B) By 3 months of age, the distribution of axon diameter returned to normal in PCC or CO treated (not shown) R98C/+ mice (P < 0.001 for both CO and PCC when compared with untreated R98C/+); the proportion of large-diameter fibres was fully corrected (n = 2–3/genotype/treatment group). (C) Increased axonal density in untreated R98C/+ mice was markedly reduced in PCC (P < 0.001) or CO (P = 0.002) treated R98C/+ animals in correlation with the increase in axon size. *P < 0.05; **P < 0.01; ***P < 0.001.
The figure legend is unchanged. It is attached below.
