Andreas Neueder

The team
The lab
Dr. Neueder successfully finished his BW-HDZ 'Baden-Württemberg-Zertifikat für Hochschuldidaktik'.
Read about it here.
Dr. Neueder became a member of the International Graduate School in Molecular Medicine Ulm (IGradU) junior faculty.
Read about it here.
Our paper showing that phenotype onset in Huntington’s disease knock-in mice is correlated with the incomplete splicing of the mutant huntingtin gene is published in the Journal of Neuroscience Research. Read it here: https://doi.org/10.1002/jnr.24493
A new review about RNA-Mediated Disease Mechanisms in Neurodegenerative Disorders is published and accessible from here:
https://doi.org/10.1016/j.jmb.2018.12.012
Our new paper about mechanisms that contribute to HTT mis-splicing got accepted by Nature Communications!
Accessible from here:
https://doi.org/10.1038/s41467-018-06281-3
Website is running
The research
(A) The CAG repeat expansion mutation in HTT leads to a polyQ tract in the HTT protein. (B) HD manifests with a triade of motor (chorea), cognitive and psychiatric symptoms.
The expanded polyQ tract of mutated HTT results in toxic gains-of-function of the protein, the generation of small fragments of HTT, the appearance of aggregates and disruption of various cellular processes. Eventually these events lead to cell death, most prominent in the neurons of the striatum.
Read more here
We have previously identified a novel mechanism that leads to the generation of the most toxic fragment of HTT: exon 1 HTT. This fragment consists only of exon 1 of the HTT gene including the polyQ tract. The generation of this fragment is based on a block in the correct splicing reaction of exon 1 HTT to exon 2 HTT. This RNA based pathogenic process occurs in all knock-in mouse models of HD, and most importantly also in human HD patients.
Read the publications here, here and here
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