[HTML][HTML] Interpretations of fundus autofluorescence from studies of the bisretinoids of the retina

JR Sparrow, KD Yoon, Y Wu… - … ophthalmology & visual …, 2010 - iovs.arvojournals.org
JR Sparrow, KD Yoon, Y Wu, K Yamamoto
Investigative ophthalmology & visual science, 2010iovs.arvojournals.org
Monitoring of monogenic and multifactorial forms of reti-nal degeneration, including age-
related macular degeneration (AMD) and some forms of retinitis pigmentosa (RP), often
includes fundus autofluorescence imaging, a modality that primarily relies on the
fluorescence generated from the bisretinoids of lipofuscin in retinal pigment epithelial (RPE)
cells. 1–3 These bisretinoids form initially in photoreceptor cells and are deposited
secondarily in the RPE. In fundus autofluorescence images, geographic atrophy (GA), and …
Monitoring of monogenic and multifactorial forms of reti-nal degeneration, including age-related macular degeneration (AMD) and some forms of retinitis pigmentosa (RP), often includes fundus autofluorescence imaging, a modality that primarily relies on the fluorescence generated from the bisretinoids of lipofuscin in retinal pigment epithelial (RPE) cells. 1–3 These bisretinoids form initially in photoreceptor cells and are deposited secondarily in the RPE. In fundus autofluorescence images, geographic atrophy (GA), and even smaller isolated patches of atrophy, can be recognized as areas of profoundly reduced fluorescence. 4, 5 Often noticed but less understood are elevated autofluorescence signals, including the high-intensity autofluorescence observed at the margin of GA4 and within the parafoveal rings of intense autofluorescence that occur in some patients with RP. 5 In this article, we visit factors that can contribute to fundus hyperautofluorescence and we provide evidence that the amount of lipofuscin in RPE cells is not the only factor governing fundus autofluorescence intensity. Photooxidation of RPE lipofuscin can also result in heightened fluorescence emission. In addition, we propose that impaired handling of vitamin A aldehyde in the setting of RPE and photoreceptor cell dysfunction and atrophy can result in excessive production of bisretinoid fluorophores in photoreceptor cells, such that these cells become an anomalous yet major source of fundus autofluorescence. The relevance of these issues to fundus autofluorescence in AMD and monogenic retinal disorders is discussed.
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