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Bascom Palmer Eye Institute

Vittorio Porciatti, D.Sc.

General Information

Vittorio Porciatti, D.Sc.

Research Subject

Prevention of Visual Dysfunction

Vision Science Focus

Visual Neurophysiology, Optic Neuropathies

Published Articles


Professor of Ophthalmology, Neuroscience and Biomedical Engineering Director, Vice Chairman of Research, and James L. Knight Professorship in Ophthalmology


Death of retinal ganglion cells (RGCs) is the cause of blindness in glaucoma and of optic nerve diseases. The central idea of Dr. Porciatti’s research is that RGCs undergo a stage of reversible dysfunction before dying. If neuronal dysfunction is detected early, then visual loss can be timely prevented and neural function restored. Dr. Porciatti’s laboratory uses non-invasive electrophysiologic and imaging techniques in human and mouse models to investigate how RGCs become dysfunctional, how and when they become susceptible to stress, and how their function may be improved.

RGC Graph

Current Research

Reversible/preventable dysfunction in glaucoma and optic nerve diseases

The fundamental tool in Dr. Porciatti’s laboratory is the pattern electroretinogram (PERG), which measures non-invasively the electrical activity of retinal ganglion cells (RGCs). The PERG is used in clinical and experimental models of diseases to 1) detect early RGC dysfunction, 2) monitor its progression, 3) assess susceptibility of RGC function to eye pressure and metabolic stress, 4) assess reversibility of RGC dysfunction after therapy. In combination with imaging, histologic, molecular and genetic approaches, a comprehensive evaluation of RGC function provides critical information on the survival mechanisms of injured RGCs, predicts their lifespan with or without therapeutic intervention, and the time window to rescue dysfunctional RGCs.

The PERG depends on the integrity of RGCs. When
the optic nerve is lesioned, RGCs degenerate and
the PERG is no longer recordable. From PNAS, 1996

RGC Table
When RGCs are exposed to a visual stimulus, they generate electric signals that require substantial metabolic energy. At any given time, the energy available to RGCs depends on the balance between energy flows originating from blood vessel and glial stores, and energy consumption of RGCs and glial cells. From Vision Res 2009