Dr. Gramlich - Center for the Prevention and Treatment of Visual Loss
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Center for the Prevention and Treatment of Visual Loss

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Dr. Gramlich

 

 
 

 

Oliver W. Gramlich, Ph.D.

Investigator, Center for the Prevention and Treatment of Visual Loss

Phone: (319) 335-7537

E-mail: oliver-gramlich@uiowa.edu

Education

MS, Zoology, Gutenberg University

PhD, Neurobiology, Gutenberg University

Post Doctural, Ophthalmology, Gutenberg University


Research Interests

The degeneration of the optic nerve is a major hallmark of optic neuropathies and demyelinating disorders such as glaucoma or multiple sclerosis (MS). Two cells are vital to the transport of visual information through the optic nerve from the retina to the brain: retinal ganglion cells and oligodendrocytes. Retinal ganglion cells are the neurons which form the axons of the optic nerve, and oligodendrocytes wrap those axons with their insulating, cholesterol-rich myelin sheath. Chronic stress to either or both cell types ultimately leads to the death of retinal ganglion cells causing permanent vision loss and blindness.

My research aims are to determine the pathobiology of initial neuroinflammatory processes leading to retina ganglion cell and oligodendrocyte degeneration using human donor tissue, animal models, and in vitro systems. I am focused on discovering new stem-cell and drug-based approaches for rehabilitation of vision loss with rapid translation of new findings into clinical practice.

My current projects are tailored to investigate how activation of the complement system and immune cells impair GABAergic and glutamatergic signaling pathways and accelerate retinal ganglion cell death in glaucoma. The goal is to inhibit the incipient inflammation and to supplement the high energy demands of retinal ganglion cells to restore their function and prevent cell death. The rehabilitation of retinal ganglion cells leads to improvement of visual acuity and will finally lessen visual field deficits.

In MS, one key opportunity for rehabilitation is the repair of the myelin sheath after an immune cell attack. I work on augmentation to increase cholesterol recycling and fatty acid metabolism providing the highly demanded energy to maintain signal transduction through the optic nerve and material for re-assembling the damaged myelin sheath. The strengthening of signal transduction in denuded axons significantly increases the likelihood of oligodendrocyte precursor cell differentiation and remyelination of those axons. Encouraging remyelination in MS improves conduction speed and will determine the magnitude of rehabilitation.