More evidence that the +1 mutations causes cell dysfunction.

View all comments by Eddie Koo

Currently there are around 20 different putative contributors related to the neuropathogenesis of Alzheimer’s disease (see ARF Current Hypotheses). In the paper by Konishi, et al., two of them are linked, i.e., frameshift and complement proteins. Several years ago, in discussions with Piet Eikelenboom (see Glia 40,232-239, 2002), we anticipated that frameshift proteins would show up earlier in postmortem material than complement proteins; aberrant proteins that can be the result of proteasome inhibition by UBB+1 (see Lindsten et al., 2002) may somehow give rise to an immune response. This idea has been worked out in the present paper, and has indeed been confirmed. It will be interesting to see if more attempts such as this (if possible, and not only in postmortem tissue!) will be made.

View all comments by Fred van Leeuwen