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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.
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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.
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.
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.
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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