Neurotrophic keratopathy (NK) is a degenerative corneal disease resulting from reduced innervation of the cornea. The loss of sensory corneal innervation can be caused by damage to the sensory 1st branch of the fifth cranial nerve (trigeminal nerve) along its entire length (from the ganglion gasseri in the brain stem) to its course in the cornea. Various diseases can lead to this damage, such as systemic diseases (diabetes mellitus, multiple sclerosis) or various infections of the cornea (herpes zoster or herpes simplex). Chemical accidents and physical trauma can also lead to damage to the trigeminal nerve , as can surgical procedures (e.g. penetrating keratoplasty) or neurosurgical procedures. As a result of the damage, the epithelial healing capacity of the cornea is often impaired with a reduction in tear secretion (sicca symptoms) and a reduction or complete loss of corneal sensitivity. Damage to the corneal nerves can lead to corneal epithelial defects, ulcers and even perforations.

The treatment of NK depends on the severity and aims to stop the progression of corneal damage and promote epithelial wound healing. Current standard therapies include topical administration of steroid eye drops, administration of artificial tears or therapeutic contact lenses. In severe cases of NK, when a corneal ulcer with perforation has developed, a lamellar or penetrating keratoplasty may be necessary. However, the success rate of corneal transplants is very low due to the poor wound healing of the epithelium and the ongoing risk of an epithelial defect. The only curative therapy option to date is treatment with the recombinant growth factor NGF (Cenegermin). Due to the high cost and limited clinical experience with this drug, cenegermin is used in patients with the most severe form of NK and the need for new forms of therapy for NK remains great.

The aim of this project is to achieve an improvement in the treatment of neurotrophic keratopathy by improving corneal nerve regeneration. Therefore, the discovery of new regeneration-associated factors and the investigation of underlying mechanisms are at the centre of the research.

As there are currently no in vitro models for testing corneal nerve regeneration, new 3D in vitro corneal models are also being generated. Artificial materials are used for these models, which are currently being investigated in our working group as replacement tissue for ocular surface reconstruction.

In addition, a mouse model of neurotrophic keratopathy has already been successfully developed, which makes it possible to verify the effectiveness of the substances found in vivo.