CIN Members

In 2007, the CIN started with 25 principal investigators as cluster applicants, as stipulated in the DFG call for bids. When the CIN cluster was approved further  scientists from a range of institutions were incorporated, to make up the 48 'founding members' of the CIN. Since the beginning of 2014 the CIN has consisted of over 80 scientists in total. The membership process involves an application to the steering committee in which the candidate outlines his or her scientific profile and submits a list of publications. The committee's decision is based purely on the scientific excellence of each candidate.

CIN Members

Prof. Dr.-Ing. Mathias Seeliger

Organization: University Hospital Tübingen, Institute for Ophthalmic Research


Schleichstr. 4
72076 Tübingen

Phone number: +49 (0)7071 29 80718

Department: Division of Ocular Neurodegeneration

Position: Heisenberg Professor

Area: CIN Members

Scientific topic: Retinal Neurodegeneration and Molecular Therapy

Field of Research

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.


Functional assessment: Electroretinography (ERG). Morphological techniques: Scanning-laser Ophthalmoscopy (SLO), Optical Coherence Tomography (OCT), Microscopy. Molecular Biology: PCR, Sequencing. Therapy: Gene Therapy, Hematopoietic Stem Cells, Microbeads


degeneration / regeneration; molecular therapy; neuro-genetics; ophthalmology; visual system

  1. Fischer MD, Huber G, Beck SC, Tanimoto N, Muehlfriedel R, Fahl E, Grimm C, Wenzel A, Remé CE, van de Pavert SA, Wijnholds J, Pacal M, Bremner R, Seeliger MW (2009). Noninvasive, in vivo Assessment of Mouse Retinal Structure Using Optical Coherence Tomography. PLoS One. 4(10):e7507.
  2. Janssen A, Min SH, Molday LL, Tanimoto N, Seeliger MW, Hauswirth WW, Molday RS, Weber BH (2008). Effect of late-stage therapy on disease progression in AAV-mediated rescue of photoreceptor cells in the retinoschisin-deficient mouse. Mol Ther. 16(6):1010-7.
  3. Seeliger MW, Grimm C, Stahlberg F, Friedburg C, Jaissle G, Zrenner E, Guo H, Remé CE, Humphries P, Hofmann F, Biel M, Fariss RN, Redmond TM, Wenzel A (2001). New views on RPE65 deficiency: the rod system is the source of vision in a mouse model of Leber congenital amaurosis. Nat Genet. 29(1):70-4.