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Complement-associated deposits in the human retina.

Aditya Seth1, Jing Cui, Eleanor To

  • 1Department of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, BC, Canada.

Investigative Ophthalmology & Visual Science
|February 1, 2008
PubMed
Summary
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Complement activation and inflammation increase with age in the human retina. Amyloid precursor protein (APP) and microglial markers suggest these processes are linked to aging, not scavenger receptor CD36.

Area of Science:

  • Ophthalmology
  • Immunology
  • Neuroscience

Background:

  • The aging human retina undergoes changes that can impact vision.
  • Complement activation and inflammation are implicated in retinal aging, but their specific mechanisms are not fully understood.

Purpose of the Study:

  • To investigate complement activation and associated inflammatory mechanisms in normal, aged human retina.

Main Methods:

  • Assessed complement activation and inflammatory markers (C5b-9, CD11b, APP, CD36, RCA-I) in 52 human retinas categorized by age (<56 and >69 years).
  • Utilized immunohistochemistry with specific antibodies and lectin binding.

Main Results:

  • Age-dependent increases in membrane attack complex (C5b-9), amyloid precursor protein (APP), microglial marker (CD11b), and lectin RCA-I immunoreactivity were observed.

Related Experiment Videos

  • C5b-9, APP, and CD11b showed robust staining in specific retinal layers (Bruch membrane, retinal pigment epithelium, choriocapillaris) in older eyes.
  • CD36 immunoreactivity was not age-dependent.

    • Conclusions:

    • Robust APP staining in older retinas suggests amyloid-beta peptides may trigger complement activation during normal aging.
    • Increased microglial markers (CD11b, RCA-I) indicate a concurrent inflammatory response to complement deposits.
    • The lack of age-dependent CD36 expression suggests other receptors mediate amyloid-beta interactions in complement activation.