June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Melanopsin ganglion cell function in early age-related macular degeneration
Author Affiliations & Notes
  • Michelle Lorraine Maynard
    Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia
  • Andrew J Zele
    Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia
  • Beatrix K Feigl
    Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia
    Queensland Eye Institute, Brisbane, QLD, Australia
  • Footnotes
    Commercial Relationships Michelle Maynard, None; Andrew Zele, None; Beatrix Feigl, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 5572. doi:
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    • Get Citation

      Michelle Lorraine Maynard, Andrew J Zele, Beatrix K Feigl; Melanopsin ganglion cell function in early age-related macular degeneration. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5572.

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

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Abstract

Purpose: Melanopsin-expressing retinal ganglion cells (mRGCs) have non-image forming functions including mediation of the pupil light reflex (PLR). There is limited knowledge about mRGC function in retinal disease. Initial retinal changes in age-related macular degeneration (AMD) occur in the paracentral region where mRGCs have their highest distribution, making them vulnerable during disease onset. In this cross-sectional clinical study, we measured the PLR to determine if mRGC function is altered in early stages of macular degeneration.

Methods: Pupil responses were measured in 8 early AMD patients (AREDS 2001 classification; mean age 72.6 ± 7.2 years, 5M and 3F) and 12 healthy control participants (mean age 66.6 ± 6.1 years, 8M and 4F) using a custom-built Maxwellian-view pupillometer. Stimuli were 0.5 Hz sinewaves (10 s duration, 35.6° diameter) of short wavelength light (464nm, blue; retinal irradiance = 14.5 log quanta.cm-2.s-1) to produce high melanopsin excitation and of long wavelength light (638nm, red; retinal irradiance = 14.9 log quanta.cm-2.s-1), to bias activation to outer retina and provide a control. Baseline pupil diameter was determined during a 10 s pre-stimulus period. The post illumination pupil response (PIPR) was recorded for 40 s. The 6 s PIPR and maximum pupil constriction were expressed as percentage baseline (Mean ± SD) and the mean difference (± SD) in phase amplitude percentage (PAP) between blue and red stimuli was calculated.<br /> .

Results: The blue PIPR was significantly less sustained (p<0.01) in the early AMD group (75.49 ± 7.88%) than the control group (58.28 ± 9.05%). The red PIPR was not significantly different (p>0.05) between the early AMD (84.79 ± 4.03%) and control groups (82.01 ± 5.86%). Maximum constriction amplitude in the early AMD group for blue (43.67 ± 6.35%) and red (48.64 ± 6.49%) stimuli were not significantly different to the control group for blue (39.94 ± 3.66%) and red (44.98 ± 3.15%) stimuli (p>0.05). The PAP difference in the early AMD group (4.49 ± 1.85%) was lower than the control group (6.53 ± 3.49%).

Conclusions: These results are suggestive of inner retinal mRGC deficits in early AMD. This non-invasive, objective measure of pupil responses may provide a new method for quantifying mRGC function and monitoring AMD progression.

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