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The short\u2010wavelength autofluorescence (SW\u2010AF) of fundus flecks in recessive Stargardt disease (STGD1) suggests a connection to these fluorophores. Through multimodal imaging, we sought to elucidate this link. Flecks observed in SW\u2010AF images often colocalized with foci exhibiting reduced or absent near\u2010infrared autofluorescence signal, the source of which is melanin in retinal pigment epithelial (RPE) cells. With serial imaging, changes in near\u2010infrared autofluorescence (NIR\u2010AF) preceded the onset of fleck hyperautofluorescence in SW\u2010AF images and fleck profiles in NIR\u2010AF images tended to be larger. Flecks in SW\u2010AF and NIR\u2010AF images also corresponded to hyperreflective lesions traversing photoreceptor\u2010attributable bands in horizontal SD\u2010OCT scans. The hyperreflective lesions interrupted adjacent OCT reflectivity bands and were associated with thinning of the outer nuclear layer. These SD\u2010OCT findings are attributable to photoreceptor cell degeneration. Progressive increases and decreases in the SW\u2010AF intensity of flecks were evident in color\u2010coded quantitative fundus autofluorescence maps. In some cases, flecks appeared to spread radially from the fovea to approximately 8\u00b0 of eccentricity, beyond which a circumferential spread characterized the distribution. Since the NIR\u2010AF signal is derived from melanin and loss of this autofluorescence is indicative of RPE atrophy, the SW\u2010AF of flecks cannot be accounted for by bisretinoid lipofuscin in RPE. Instead, we suggest that the bisretinoid serving as the source of the SW\u2010AF signal, resides in photoreceptors, the cell that is also the site of bisretinoid synthesis.<\/jats:p>","DOI":"10.1002\/jnr.24252","type":"journal-article","created":{"date-parts":[[2018,4,27]],"date-time":"2018-04-27T11:08:16Z","timestamp":1524827296000},"page":"98-106","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["Photoreceptor cells as a source of fundus autofluorescence in recessive Stargardt disease"],"prefix":"10.1002","volume":"97","author":[{"given":"Maarjaliis","family":"Paavo","sequence":"first","affiliation":[{"name":"Department of Ophthalmology Columbia University Medical Center New York New York"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Winston","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology Columbia University Medical Center New York New 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