Seeliger Lab

Ocular Neurodegeneration

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Research Projects

Neuro-Imaging (SLO, OCT)

Establishment of Scanning Laser Ophthalmoscopy (SLO) and Optical Coherence To-mography (OCT) in experimental imaging. Replacement of conventional histology by in vivo imaging, specific in vivo follow-up of individual cells via transgenic expression of marker proteins like Green Fluorescent Protein (GFP).

Retinal Neurodegeneration Research

Several projects aiming at the detection of retinal pathophysiology in inherited retinal degenerations, which are among the most common causes of adult blindness. Trans-genic models are used to uncover the disease mechanisms underlying inherited neurodegenerative diseases. Examples: the rd1 mouse model featuring a dysfunction of photoreceptor PDE (phosphodiesterase) and Crumbs complex mutants.

Molecular Therapy Research

In collaboration with the group of Martin Biel, Pharmacology, LMU München, we devel-oped and implemented novel therapeutic strategies. Using gene therapy, we obtained clear functional and morphological rescue in a channelopathy (Cnga3). We now work on the translation to human patients with achromatopsia. Further, CellBeads, live cells encapsulated in an alginate sphere that produce neuroprotective factors, are also a promising approach.

Systems Biology of Retinal Function

The goal is to gain a deeper insight in the complex system „Retina“ based on data from the human disease and the respective animal models that allows for modelling patho-physiological processes and eventually may be the foundation for an educated therapy. Examples: Mesopic functional interdependencies between rod and cone systems in normal retina based on Hcn1/Cx36 mutant mice, the role of Creatin kinase, and detection of the target of pathologically high cGMP levels in rd1.

Future Development

The current work as described in detail above is to be continued, with a special emphasis on the exposure of retinal functional interdependencies and the establish-ment of innovative therapeutic strategies. In the latter area, we just recently obtained new data in a model of Retinitis Pigmentosa due to a loss of the gene for CNGB1, which suggest a similarly effective rescue as in the case of achromatopsia.