September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Neuronal Gap Junctions form Novel Therapeutic Targets for Neuroprotection in Glaucoma
Author Affiliations & Notes
  • Stewart A Bloomfield
    Biological and Vision Sciences, State University of New York College of Optometry, New York, New York, United States
  • Footnotes
    Commercial Relationships   Stewart Bloomfield, None
  • Footnotes
    Support  NIH Grant EY007360
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Stewart A Bloomfield; Neuronal Gap Junctions form Novel Therapeutic Targets for Neuroprotection in Glaucoma. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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      © ARVO (1962-2015); The Authors (2016-present)

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Presentation Description : The death of retinal ganglion cells is a hallmark of glaucoma, which leads to diminished visual function. In addition to the well-characterized intracellular cascades responsible for primary cell death, intercellular movement of toxic molecules via gap junctions between dying neurons and their neighbors appears to play a crucial role in the progression of cell death across the retina. This finding suggests that targeting neuronal gap junctions forms a novel therapeutic strategy for neuroprotection in glaucomatous retinas to thereby preserve visual function.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.


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