Dr. Bettina Schmid

Group Leader
The Fish Core Facility is associated to Prof. Dr. Haass chair

German Center for Neurodegenerative Diseases (DZNE)
Feodor-Lynen-Str. 17
81377 Munich

bettina.schmid@dzne.de
+49 (0) 89 / 4400-46511
+49 (0) 89 / 4400-46508

Group members

Name Phone Fax
Frauke van Bebber, Ph.D., Postdoc +49 (0)89/4400-46513 +49 (0)89/4400-46508
Dr. Sven Lammich, Postdoc
Alexander Hruscha, Technical Assistant +49 (0)89/4400-46512 +49 (0)89/4400-46508
Esau Roberto Rojas Rojas, Animal Keeper +49 (0)89/4400-46449 +49 (0)89/4400-46508
Further group members (LMU/third party funding)
Barbara Solchenberger, Ph.D. student +49 (0)89/2180-75490 +49 (0)89/4400-46508
Laura Hasenkamp, Ph.D. student +49 (0)89/4400-46514 +49 (0)89/4400-46508
Click on the magnifying glass for a large image.

Selected Publications

Highly Efficient Targeted Mutagenesis in Mice Using TALENs.

Panda SK, Wefers B, Ortiz O, Floss T, Schmid B, Haass C, Wurst W, Kühn R. Genetics. 2013 Aug 26.  

Analysis of BACE1 and BACE2 in zebrafish reveal non redundant functions.

van Bebber F, Hruscha A, Willem M, Schmid B*, and Haass C*. J Neurochem. 2013 Feb 14. *equal senior authors  

Dual cleavage of Neuregulin 1 type III by BACE1 and ADAM17 liberates its EGF-like domain and allows paracrine signaling.

Daniel Fleck, Frauke van Bebber, Alessio Colombo, Chiara Galante, Benjamin Schwenk, Linnea Rabe, Heike Hampel, Bozidar Novak, Elizabeth Kremmer, Sabina Tahirovic, Dieter Edbauer, Stefan Lichtenthaler, Bettina Schmid, Michael Willem, and Christian Haass. J Neurosci. 2013 May 1;33(18):7856-69. 

Label-free quantitative analysis of the membrane proteome of Bace1 protease knock- out zebrafish brains.

Hogl S, van Bebber F, Dislich B, Kuhn P-H, Haass C, Schmid B, and Lichtenthaler SF. Proteomics. 2013 May;13(9):1519-27. 

Mutations in ap1b1 cause mistargeting of the Na+/K+-ATPase pump in sensory hair cells.

Clemens-Grisham R, Katie Kindt K, Finger-Baier K, Schmid B, Nicolson T. PLoS One. 2013 Apr 12;8(4):e60866. 

The Expanded GGGGCC Repeat in C9orf72 is Translated into Aggregating Dipeptide-Repeat Proteins in FTLD/ALS.

Mori K, Wenig S-M, Arzberger T, May S, Rentzsch K, Kremmer E, Schmid B, Kretzschmar HA, Cruts M, Van Broeckhoven C, Haass C, Edbauer D. Science. 2013 Mar 15;339(6125):1335-8. 

Loss of TDP-43 causes hypoperfusion and muscle dystrophy.

Schmid B, Hruscha A, Hogl S, Strathmann J, van der Zee J, Teucke M, Eimer S, Hegermann J, Kittelmann M, Kremmer E, Cruts M, Solchenberger B, Hasenkamp L, Strecker K, van Bebber F, Van Broeckhoven C, Edbauer D, Lichtenthaler S, Haass C. Proc Natl Acad Sci U S A. 2013 Mar 26;110(13):4986-91. 

In vivo imaging of disease-related mitochondrial dynamics in a vertebrate model system.

Plucińska D, Paquet D, Hruscha A, Godinho L, Haass C, Schmid B*, Misgeld T*. J Neurosci. 2012 Nov 14;32(46):16203-12. *equal senior authors

Parkin is protective against proteotoxic stress in a transgenic zebrafish model.

Fett ME, Pilsl A, Paquet D, van Bebber F, Haass C, Tatzelt J, Schmid B, Winklhofer KF, PLoS One. 2010 Jul 30;5(7):e11783.

ALS-associated fused in sarcoma (FUS) mutations disrupt Transportin-mediated nuclear import.

Dormann D, Rodde R, Edbauer D, Bentmann E, Fischer I, Hruscha A, Than ME, Mackenzie IR, Capell A, Schmid B, Neumann M, Haass C, EMBO J. 2010 Aug 18;29(16):2841-57. Epub 2010 Jul 6.

Methylene blue fails to inhibit Tau and polyglutamine protein dependent toxicity in zebrafish.

van Bebber F, Paquet D, Hruscha A, Schmid B, Haass C, Neurobiol Dis. 2010 Sep;39(3):265-71. Epub 2010 Apr 8.

Transgenic zebrafish as a novel animal model to study tauopathies and other neurodegenerative disorders in vivo.

Paquet D, Schmid B, Haass C, Neurodegener Dis. 2010;7(1-3):99-102. Epub 2010 Feb 18.

A zebrafisch model of tauopathy allows in vivo imaging of neuronal cell death and drug evaluation.

Paquet D., Bhat R., Sydow A., Mandelkow E., Distel M., Köster R., Schmid B. and Haass C. (2009), J. Clinical Investigation, 119, 1382 - 1395.

Curriculum Vitae

Dr. Bettina Schmid studied Biology in Hohenheim, Corvallis (Oregon, USA), and Tübingen where she graduated in 1996. During her diploma work she collected the first experiences with zebrafish in the lab of Prof. Christiane Nüsslein-Volhard.  She then moved to the University of Pennsylvania (USA) (Prof. Mullins) for her PhD and graduated in 1999. After a Postdoc at Harvard Medical School (USA) with Prof. Len Zon she returned for two more years back to the Max-Planck Institute of Developmental Biology (Prof. Nicolson) in Tübingen. From 2003 until 2009 she was as a junior group leader at the Ludwig-Maximilians-Unversität in the Department of Prof. Christian Haass. She established a Zebrafish faclity and a research group focussing on neurodegenerative diseases in Zebrafish.

She has been the leader of the Zebrafish Core Facility of the DZNE since November 2009.


Areas of investigation/research focus

Our group uses the advantages of the zebrafish, Danio rerio, as an in vivo model system to address some of the unresolved questions in Alzheimer’s disease, Parkinson’s disease, Frontotemporal Lobar Degeneration (FTLD), and Amyotrophic lateral Sclerosis (ALS). Our research has four major aims:

  • Generation of transgenic zebrafish
    Animal models are crucial in understanding disease mechanisms and to design therapeutic strategies. We generated a powerful Gal4-UAS based trangenesis vector system that allowed us to generate numerous transgenic zebrafish lines. Transgenic expression of human disease associated genes enables us to recapitulate hallmarks of the respective human disease in zebrafish.
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  • Generation of knock-downs and mutants
    Genes associated with neurodegenerative diseases are being investigated for their in vivo function in zebrafish. Interestingly, very little is known about the physiological function of genes such as TDP-43 - despite their well-established role in ALS and FTD. Manipulation of protein levels mediated by injection of antisense gripNAs and subsequent analysis of the generated phenotypes enable us to gain insight into their physiological function. Additionally mutations in disease relevant genes are currently established by zinc finger nuclease mediated genome editing.  
  • In vivo imaging
    One of the great advantages of the zebrafish is the optical transparency during early larval stages. This allows expression of fluorescent reporters and in vivo imaging at sub-cellular resolution.  For example, we were able to image neuronal cell death in Tg(HuC:TauP301L) larvae in vivo.  
  • Drug evaluation in disease models
    The transgenic disease models generated are great tools to search for disease modifying drugs. Zebrafish larvae are small in size (< 1mm) and live in an aqueous environment where chemicals can be easily applied. Zebrafish therefore represent a wonderful tool to assay for disease modifying drugs in vivo.

The cooperation partner's homepage can be found here.