Institute for Ophthalmic Research

Head

Prof. Dr. med. Dipl.-Ing. Mathias Seeliger

Contact

Schleichstr. 4/3
72076 Tuebingen

Phone +49 7071 29-80718 
Email see [at] uni-tuebingen [dot] de

Mission statement

Our mission is to uncover the pathophysiology of ocular neurodegenerative processes, to develop and test therapeutic strategies and to understand and model normal retinal function. The basis of our work is in-depth functional and morphological phenotyping of genetic models of blinding human neurodegenerative disorders with electroretinography (ERG), scanning-laser ophthalmoscopy (SLO), and optical coherence tomography (OCT), the same non-invasive techniques used in affected patients.

Main fields of work

• Neurodegeneration research: We investigate the causes of and the disease mechanisms in retinal degenerations, and relate the findings in human patients to those in animal models with homologous genetic defects. Also, we examine animal models generated by groups worldwide for their relevance in this regard.
• System biology: As many aspects of normal retinal function are still unclear, we assess functional pathways, particularly in the outer retina, by means of mouse lines with specific genetic defects in photoreceptor function and/or connectivity. Cross-breeding of such lines enables us to investigate isolated pathways, to obtain new insights about their nature, and to model their behaviour.
• Molecular therapy: Recent advances in therapeutic research (particularly gene and stem cell therapy) have led to collaborations with many leading groups on the evaluation of therapy in affected models. Our main field is the development of optimal application procedures and the evaluation of the therapeutic success by short- and long-term follow-up in vivo.
• Methodological innovation and refinement: Since more than a decade, we are involved in the development and refinement of innovative diagnostic strategies in human patients and animal models. In addition, we are regularly contributing to ERG standards/guidelines issued by the International Society for Clinical Electrophysiology of Vision (ISCEV).

Selected publications

Seeliger MW, Grimm C, Ståhlberg F, Friedburg C, Jaissle G, Zrenner E, Guo H, Remé ChE, Humphries P, Hofmann F, Biel M, Fariss RN, Redmond TM, Wenzel A. New views on RPE65 deficiency: the rod system is the source of vision in a mouse model of Leber congenital amaurosis. Nat Genet 2001; 29: 70-74.

Grimm C, Wenzel A, Groszer M, Mayser H, Seeliger MW, Bauer C, Gassmann M, Reme CE. HIF-1-induced erythropoietin in the hypoxic retina protects against light-induced retinal degeneration. Nat Med 2002; 8: 718-24.

Tolmachova T, Anders R, Abrink M, Bugeon L, Dallman MJ, Futter
CE, Ramalho JS, Tonagel F, Tanimoto N, Seeliger MW, Huxley C, Seabra MC. Cell-autonomous retinal degeneration in a conditional knockout mouse model of choroideremia. J Clin Invest 2006; 116: 386- 394.

Bemelmans AP, Kostic C, Crippa SV, Hauswirth WW, Lem J, Seeliger MW, Wenzel A, Arsenijevic Y. Lentiviral-mediated transfer of the RPE65 cDNA rescues both survival and function of cone photoreceptors in a mouse model of Leber congenital amaurosis. PLoS Med 2006; 3: 1892-1903.

Hirzel K, Mueller U, Latal UT, Huelsmann S, Grudzinska J, Seeliger MW, Betz H, Laube B. Hyperekplexia phenotype of glycine receptor a1 subunit mutant mice identifies Zn2+ as an essential endogenous modulator of glycinergic neurotransmission. Neuron 2006; 52: 679-690.