Andreas Neueder
THE LAB
Read news from the lab and our publications, meet our funding bodies and find open positions in the lab.
The team
current and former lab members
Nathalie Birth (technician)
Nousheen Iram-Muehlinghaus (postdoc, 2020 - current)
Alshaimaa Abdelmoez (postdoc, 2019 - current)Franziska Hoschek (Dr. rer. nat., 2019 - current)
Judith Rammoser (Dr. med., 2019 - current)
Julia Hummel (Dr. med., 2019 - current)
Philipp Nitzschner (Dr. med., 2019 - current)
Franziska Hoschek (MSc, 2019)
Open positions
If you are intersted in our work and would like to be part of the team, please contact us.
The lab
News - 2020
BW-HDZ teaching certificate
Dr. Neueder successfully finished his BW-HDZ 'Baden-Württemberg-Zertifikat für Hochschuldidaktik'.
Read about it here.
News - 2019
Junior faculty
Dr. Neueder became a member of the International Graduate School in Molecular Medicine Ulm (IGradU) junior faculty.
Read about it here.
Paper got Published
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
Review got Published
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
News - 2018
Paper got accepted!
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 created
Website is running
Funding bodies
The research
Huntington's Disease (HD)
(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.
Background
Huntington’s disease (HD) was first described in 1872 by George Huntington and is a late-onset, autosomal dominant, inherited neurodegenerative disorder. It is caused by a CAG repeat expansion mutation in exon 1 of the HTT gene resulting in an expanded polyglutamine (polyQ) tract in the huntingtin protein.
Read more here
Read more here
Molecular Changes
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
Exon 1 HTT
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
The Projects
We use a combination of molecular biology and systems biology approaches to unravel mechanisms driving HD pathogenesis.
Generation of novel models
We design, establish and analyse new models for certain aspects of pathogenetic mechanisms in HD.
'omics
We generate and analyse 'big data' in the context of HD. These datasets come from various biological sources and we use advanced network based bioinformatics to evaluate and integrate the 'omics datasets.
RNA biology
We are interested in the contribution of RNA based mechanisms to cell (type specific) toxicity in HD. In particluar we try to unravel mechanisms that contribute to the incomplete splicing of the HTT mRNA.
Collaborations
contact
Address
Department of Neurology
Ulm University
Helmholtzstrasse 8/1 ZBMF, room 0.23
89081 Ulm, Germany
Ulm University
Helmholtzstrasse 8/1 ZBMF, room 0.23
89081 Ulm, Germany
Phone number
+49 (0)731 500 63117
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