Welcome to the Neueder lab!

We are interested in neurodegenerative diseases.
We are interested in RNA biology.
We use a combination of molecular and systems biology approaches
to gain insights into disease mechanism.




Read news from the lab and our publications, meet our funding bodies and find open positions in the lab.


Discover our research projects and learn about the methods we are using.


Meet the people in the lab.


Address, directions and other contact details.

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.

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

News - 2018

website created

Website is running


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.

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

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

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.
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.


UCL, UK    Bates lab    read more

UCL, UK  Tabrizi lab    read more

Ulm, D    Landwehrmeyer lab    read more

Würzburg, D    Braunger lab    read more

UPenn, US    Davidson lab     read more

Michigan, US   Lieberman  lab     read more

Emory, US    Li lab    read more

IGBMC, F    Trottier lab    read more

LNCA, F    Merienne lab    read more


Department of Neurology
Ulm University
Helmholtzstrasse 8/1 ZBMF, room 0.23
89081 Ulm, Germany

Phone number

+49 (0)731 500 63117

Find us