July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Galantamine confers neuroprotection in a model of indirect traumatic optic neuropathy
Author Affiliations & Notes
  • Sarah Naguib
    Vanderbilt University, Nashville, Tennessee, United States
    Vanderbilt University Medical Center, Tennessee, United States
  • Alexandra Bernardo-Colon
    Vanderbilt University Medical Center, Tennessee, United States
  • Caroline Cencer
    Vanderbilt University, Nashville, Tennessee, United States
  • Tonia S Rex
    Vanderbilt University Medical Center, Tennessee, United States
    Vanderbilt University, Nashville, Tennessee, United States
  • Footnotes
    Commercial Relationships   Sarah Naguib, None; Alexandra Bernardo-Colon, None; Caroline Cencer, None; Tonia Rex, None
  • Footnotes
    Support  DoD W81XWH-15-1-0096, W81XWH-17-2-0055, NEI R01 EY022349, NEI P30 EY008126, NIA R01 NS094595, Research to Prevent Blindness Unrestricted Funds (P. Sternberg), Ret. Maj. General Stephen L. Jones, MD Fund, Mark Pigott Fund,Potoscnak Family-CSC Research Fund, Ayers Research Fund in Regenerative Visual Neuroscience, NIH T32 Training Grant in Vision Research
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 4407. doi:https://doi.org/
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      Sarah Naguib, Alexandra Bernardo-Colon, Caroline Cencer, Tonia S Rex; Galantamine confers neuroprotection in a model of indirect traumatic optic neuropathy . Invest. Ophthalmol. Vis. Sci. 2019;60(9):4407. doi: https://doi.org/.

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

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Abstract

Purpose : Our goal was to investigate the neuroprotective effects of galantamine, an FDA-approved mild Alzheimer’s Disease treatment, in a mouse model of blast-induced traumatic optic neuropathy.

Methods : We exposed one eye of an anesthetized mouse to two bursts of over-pressurized air, 0.5 seconds apart for three days in a row. Blast and sham mice were given either regular or galantamine water (120mg/L) ad libitum, beginning immediately after blast and continuing for one month. Electrophysiology and optical coherence tomography were performed 1 month after injury. Optic nerve and retina histology, ELISAs, TUNEL, Western blot, and immunohistochemistry were performed to assess oxidative stress, inflammation, cell death, and synaptic changes.

Results : Galantamine treatment preserved visual function based on ERG and VEP. Injury did not affect the amax, however it significantly decreased the bmax from 246 ± 37 mV to 157 ± 41 mV. Galantamine treatment preserved the bmax to 198 ± 22 mV. Similarly, injury reduced the amplitude of the VEP N1 from 43 ± 10 mV to 26 ± 6.4 mV, which was ameliorated by galantamine treatment (36 ± 7.6 mV). Galantamine preserved retinal synaptic overlap in the outer plexiform layer based on immunolabeling of synaptophysin and calbindin-D or PKCα. Galantamine also prevented axon degeneration in the optic nerve. Further, galantamine preserved SOD2 levels and prevented blast-induced increases in IL-1α and IL-1β.

Conclusions : Post-injury treatment with galantamine after injury is effective in protecting the retina and optic nerve and preserving vision. Galantamine may be a promising treatment for indirect traumatic optic neuropathy.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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