An excellent update of the recent findings on TDP-43 and progranulin in FTD.

View all comments by Jurgen Goetz

With regard to a possible genetic contribution of TDP-43 to FTLD-U, our group reported negative results in Salzburg. We conducted a high-density genetic association and linkage disequilibrium mapping analysis to investigate whether common variations at the TDP-43 locus act as a risk factor for disease in the Manchester FTLD cohort. Among 214 patients not harboring a tau or progranulin mutation, who were clinically diagnosed as having either FTD, FTD with motor neuron disease, semantic dementia, or related disorders, we observed no significant SNP or haplotype association (Rollinson et al., 2007, in press). These data suggest that common variations do not increase genetic risk in our population, but it leaves open the possibility of rare mutations yet to be found.

View all comments by Stuart Pickering-Brown