May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Evidence of Widespread Photoreceptor Degeneration in Aged and AMD Retinas
Author Affiliations & Notes
  • J. M. Provis
    RSBS, The Australian National University, Canberra, Australia
    ARC Centre of Excellence in Vision Science, Canberra, Australia
  • E. J. Shelley
    RSBS, The Australian National University, Canberra, Australia
  • M. C. Madigan
    University of Sydney, Save Sight Institute, Sydney, Australia
  • Footnotes
    Commercial Relationships J.M. Provis, None; E.J. Shelley, None; M.C. Madigan, None.
  • Footnotes
    Support ARC Centre of Excellence in Vision Science
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 3020. doi:
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      J. M. Provis, E. J. Shelley, M. C. Madigan; Evidence of Widespread Photoreceptor Degeneration in Aged and AMD Retinas. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3020.

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

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Purpose:: To investigate the pathology status of photoreceptors in the central retina of normal aged human retinas, and in AMD retinas.

Methods:: Eyes (>70 years) were collected with informed consent through the Lions Sydney Eye Bank, fixed in 2% paraformaldehyde, rinsed and the fundus photographed. The retina and RPE were dissected out whole, flattened, and embedded in gelatin. A gelatin block (~8 x 10 mm) including the macula and adjacent region was excised, frozen and sectioned at 10 microns. One in 60 sections was stained using haematoxylin and eosin for histopathology and two adjacent series were double immunolabeled, using standard methods, with antibodies to rhodopsin, long-medium wavelength sensitive (L/M) opsin and glial fibrillary acidic protein (GFAP). Selected sections were double immunolabeled with antibodies against synaptic vesicle protein 2, the synaptic ribbon marker CtBP2, vesicular glutamate transporter 1 (vGluT1), cone arrestin and Muller cell markers.

Results:: Two out of 8 eyes analysed had a history of AMD. By histopathology, 4 had changes consistent with AMD; three eyes were histologically normal; one had macular hole and one had unspecified pan-retinal photoreceptor degeneration. All retinas (8/8) showed evidence of widespread photoreceptor degeneration, particularly in the cone population. This included cone prolapse into the subretinal space; opsin expression in the cell membrane, axon and pedicle; axonal swelling and beading; loss of synaptic markers; low levels of arrestin; and loss of outer and inner segments. Rod pathology was evident surrounding overt histopathological lesions and the optic nerve head, and included rhodopsin expression in the soma and spherule. In histologically normal retinas the foveal region seemed somewhat protected from these changes.

Conclusions:: We identified evidence of pan-retinal degeneration of photoreceptors in a small sample of aged and AMD retinas. The results suggest that in normal aging the macula may be protected from this degeneration.

Keywords: age-related macular degeneration • aging • retina 

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