Andreas Neueder

TL;DR: It is shown that CAG repeat length–dependent aberrant splicing of exon 1 HTT results in a short polyadenylated mRNA that is translated into an exon 2 HTT protein, which provides a mechanistic basis for the molecular pathogenesis of HD.

TL;DR: The results show that key aspects of the assembly of eukaryotic r-proteins into distinct structural parts of the SSU are similar to the in vitro assembly pathway of their prokaryotic counterparts.

TL;DR: Working hypotheses are discussed on how individual r-proteins control the productive processing of the major 5′ end of 5.8S rRNA precursors by exonucleases Rat1p and Xrn1p, and the nature of structural characteristics of nascent LSUs that are required for cytoplasmic accumulation of nascent subunits but are nonessential for most of the nuclear LSU pre-rRNA processing events.

TL;DR: It is postulate that the HD-related cardiomyopathy is caused by altered central autonomic pathways although the pathogenic effects of mutant HTT acting intrinsically in the heart may also be a contributing factor.

TL;DR: Previously unidentified transcription dysregulation in the HD cerebellum was uncovered that contained a gene expression signature in common with the caudate nucleus and the BA4 region of the frontal cortex, which provided novel insights into the molecular pathogenesis in HD.