title: Topographic and age-related changes of the retinal epithelium and Bruch's membrane of rhesus monkeys.
abstract: OBJECTIVE
  To examine structural differences in the retinal pigmented epithelium (RPE) and Bruch's membrane of rhesus monkeys (Macaca mulatta) as a function of topography and age.
  
  
  METHODS
  The retinas of two old (24 and 26 years old) and two young (1 and 6 years old) female monkeys were examined by light fluorescence and electron microscopy at the macula, equator, and ora serrata.
  
  
  RESULTS
  All monkeys lacked fluorescence and lipofuscin granules in the RPE at the ora serrata where photoreceptors are absent. The equator and macula showed intense fluorescence and many lipofuscin granules in the RPE of the old but not the young monkeys. At the ora, the RPE contained many dense round melanin granules throughout the cell. At the equator and macula, melanin granules were more apical, less frequent, and often elongated. Mitochondria were clustered at the basal side of the RPE cell near infolds of the plasma membrane. Both mitochondria and infolds tended to increase toward the macula. In all regions, the basal lamina of the RPE did not penetrate the extracellular space adjacent to infolds. The elastin layer of Bruch's membrane was wide at the ora and equator and thinner at the macula. In the old monkeys, drusen were found at all retinal regions between the basal lamina and the internal collagen layer of Bruch's membrane. The drusen were often membrane-bound with a basal lamina and contained material resembling structures in the RPE.
  
  
  CONCLUSIONS
  Lack of fluorescence and lipofuscin in the RPE at the ora serrata, where photoreceptors are absent, confirms that RPE fluorescence occurs only where outer segments are phagocytized. Mitochondrial clustering indicates that the basal side of the RPE cell uses the most energy and this becomes maximal at the macula. The presence of age-related degenerative changes and drusen at all retinal locations in the older monkeys, even at the ora where RPE lipofuscin was absent, indicates that these processes are not dependent on local lipofuscin accumulation. Therefore lipofuscin toxicity may not be the sole cause of age-related RPE degeneration.
authors.affiliation: Department of Ophthalmology, Columbia University, New York, NY 10032, USA. pg10@columbia.edu
authors.forename: Peter
authors.initials: P
authors.lastname: Gouras
authors.forename: Lena
authors.initials: L
authors.lastname: Ivert
authors.forename: Martha
authors.initials: M
authors.lastname: Neuringer
authors.forename: Julie A
authors.initials: JA
authors.lastname: Mattison
mesh_terms: D000375:Aging / Q000473:pathology*; D000818:Animals; D016570:Bruch Membrane / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D002462:Cell Membrane / Q000473:pathology / Q000648:ultrastructure; D003594:Cytoplasmic Granules / Q000473:pathology / Q000648:ultrastructure; D005260:Female; D008062:Lipofuscin / Q000378:metabolism; D008253:Macaca mulatta; D008266:Macula Lutea / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D008543:Melanins / Q000378:metabolism; D046529:Microscopy, Electron, Transmission; D008856:Microscopy, Fluorescence; D008928:Mitochondria / Q000473:pathology / Q000648:ultrastructure; D012162:Retinal Degeneration / Q000378:metabolism / Q000473:pathology; D015593:Retinal Drusen / Q000378:metabolism / Q000473:pathology*; D055213:Retinal Pigment Epithelium / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure
chemical_list: D008062:Lipofuscin; D008543:Melanins