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1 ere performed on 22 eyes of 11 patients with Stargardt disease.
2 n eye cups of Abca4/Abcr-/- mice, a model of Stargardt disease.
3 s due to retinal degeneration (RD) including Stargardt disease.
4 nerate a Leu2027Phe mutation associated with Stargardt disease.
5 ce tomography) and patient data in recessive Stargardt disease.
6  function of ABCA4 and mechanisms underlying Stargardt disease.
7 r intravitreal injection in a mouse model of Stargardt disease.
8 fied in the sister originally diagnosed with Stargardt disease.
9 ains (NBDs), have been genetically linked to Stargardt disease.
10  the most common IRD encountered followed by Stargardt disease.
11 193 images from 193 eyes of 97 patients with Stargardt disease.
12 enotype of the Abca4(-/-)/Rdh8(-/-) model of Stargardt disease.
13 -p.Gly1961Glu, the most frequent mutation in Stargardt disease.
14 ogression are needed for treatment trials of Stargardt disease.
15 ubset of patients with genetically confirmed Stargardt disease.
16 mportant to understand the histopathology of Stargardt disease.
17 al end points for future treatment trials in Stargardt disease.
18 ssociated clinical findings in patients with Stargardt disease.
19 tive outcome measure for treatment trials of Stargardt disease.
20 aughters with pseudodominant transmission of Stargardt disease.
21 te to the clinical staging and monitoring of Stargardt disease.
22 l biomarker for measuring the progression of Stargardt disease.
23 ayer was observed in 8 of 41 eyes (20%) with Stargardt disease.
24 y age-related macular degeneration (AMD) and Stargardt disease.
25 ivation might be beneficial in patients with Stargardt disease.
26 g cassette (ABC) family, are associated with Stargardt disease.
27  assess whether these findings are unique to Stargardt disease.
28 trophic age-related macular degeneration and Stargardt disease.
29 rence tomography in monitoring patients with Stargardt disease.
30 s of 85 patients with molecular diagnoses of Stargardt disease.
31 pite a retinopathy otherwise consistent with Stargardt disease.
32 ective review of data from 198 patients with Stargardt disease.
33 y enlargement were observed in patients with Stargardt disease.
34 cularly age-related macular degeneration and Stargardt disease.
35 -up in a group of 12 patients (24 eyes) with Stargardt disease.
36 c age-related macular degeneration (AMD) and Stargardt disease.
37 ant in Abca4(-/-) mice, a model of recessive Stargardt disease.
38 elated probands with a clinical diagnosis of Stargardt disease, 182 patients with age-related macular
39                    Twenty-nine patients with Stargardt disease (25%) and two with CRD had no identifi
40                   Twenty-eight patients with Stargardt disease (53 eyes) with a mean age of 46 (15-79
41        Gap height decreased in patients with Stargardt disease (6.5 mum/year; P = .02) but increased
42 ges in gap width were noted in patients with Stargardt disease (78.1 mum/year) and cone dystrophies (
43 sible for the loss of RPE cells in recessive Stargardt disease, a blindness macular disorder of juven
44 od photoreceptor protein and is defective in Stargardt disease, a common hereditary form of macular d
45       Mutations in ABCA4 are responsible for Stargardt disease, a degenerative disorder associated wi
46 pharmacological targets for the treatment of Stargardt disease, a severe juvenile form of macular deg
47 sive nature of optical gaps in patients with Stargardt disease, achromatopsia, occult macular dystrop
48 ditary and sporadic retinal diseases such as Stargardt disease, age-related macular degeneration or r
49                                              Stargardt disease, also known as juvenile macular degene
50                                              Stargardt disease, an ATP-binding cassette, subfamily A,
51 tor-specific ABC transporter responsible for Stargardt disease, an early onset macular degeneration.
52         Sixteen patients with a diagnosis of Stargardt disease and a Gly1961Glu mutation were enrolle
53                       In these patients with Stargardt disease and a Gly1961Glu mutation, most showed
54 marks of various retinal diseases, including Stargardt disease and age-related macular degeneration (
55 ble genetic and age-related human disorders, Stargardt disease and age-related macular degeneration (
56  RPE is associated with pathogenesis of both Stargardt disease and age-related macular degeneration (
57 t microglial/macrophage activation in both a Stargardt disease and age-related macular degeneration m
58                                        Thus, Stargardt disease and age-related macular degeneration m
59  photodamage, especially in individuals with Stargardt disease and age-related macular degeneration t
60 lmark of aging and retinal disorders such as Stargardt disease and age-related macular degeneration.
61  similar mechanism may be operative in human Stargardt disease and age-related macular degeneration.
62 are promising for non-viral gene therapy for Stargardt disease and can be expended for applications i
63 ordance of the phenotype may be a feature of Stargardt disease and cone dystrophies.
64 tment strategy for retinal diseases, such as Stargardt disease and dry age-related macular degenerati
65 ing the visual cycle and the pathogenesis of Stargardt disease and for the identification of compound
66 ss using in vivo OCT data from patients with Stargardt disease and healthy controls.
67 ction may play a role in the pathogenesis of Stargardt disease and is evidenced in human retinas.
68 -specific flippase ABCA4 are associated with Stargardt disease and many other forms of retinal degene
69  Thirty-seven (31%) of the 118 patients with Stargardt disease and one with CRD had only one likely p
70  vitamin A can prevent vision loss caused by Stargardt disease and other retinopathies associated wit
71 es previously unexplored in the treatment of Stargardt disease and provides a surrogate assay for ass
72  the blinding degeneration characteristic of Stargardt disease and related forms of macular degenerat
73       Together with clinical observations on Stargardt disease and the localization of ABCR to rod ou
74 es in the Abca4(-/-)Rdh8(-/-) mouse model of Stargardt disease and the Mertk(-/-) mouse model of reti
75                      Out of 62 patients with Stargardt disease and wide-field retinal imaging, 14 had
76 h 36 eyes with PPS maculopathy, 50 eyes with Stargardt disease, and 40 eyes with PRPH2-associated mul
77 ital stationary night blindness (CSNB), LCA, Stargardt disease, and blue cone monochromacy.
78 ostructure on spatially-resolved function in Stargardt disease, and might be used as quasi-functional
79 eration in age-related macular degeneration, Stargardt disease, and recessive cone dystrophies is a m
80  including age-related macular degeneration, Stargardt disease, and retinitis pigmentosa.
81 es such as age-related macular degeneration, Stargardt disease, and retinitis pigmentosa.
82            Age-related macular degeneration, Stargardt disease, and their Abca4(-/-) mouse model are
83 cone-rod dystrophy (approximately 1:14 000), Stargardt disease (approximately 1:16 000), Usher syndro
84   Age-related macular degeneration (AMD) and Stargardt disease are the leading causes of blindness fo
85  retinal pigment epithelium in patients with Stargardt disease as determined by fundus autofluorescen
86  number of choroidal hyperreflective foci in Stargardt disease as well as correlation with visual acu
87                                              Stargardt disease-associated mutations in this domain re
88 ntosa with a percentage of 78.9% followed by Stargardt disease at 6.3%, cone-rod dystrophy at 2.0%, a
89 nge of inherited retinal diseases, including Stargardt disease, autosomal recessive cone rod dystroph
90 f inherited macular degenerations, including Stargardt disease, autosomal recessive cone rod dystroph
91 k of major degenerative eye diseases such as Stargardt disease, Best disease, and age-related macular
92 cular degeneration, including juvenile onset Stargardt disease, Best vitelliform macular degeneration
93 gs were compared with those of patients with Stargardt disease but no foveal sparing.
94                         In the 10 studies on Stargardt disease, choroidal hyperreflective foci were p
95 ients who had been clinically diagnosed with Stargardt disease, cone-rod dystrophy, and other ABCA4-a
96  segmentation of autofluorescence lesions in Stargardt disease, demonstrating the feasibility of full
97 lysis of a larger cohort of individuals with Stargardt disease did not support the association betwee
98 ic (ERG) studies indicate that patients with Stargardt disease exhibit abnormally slow rod dark adapt
99 otentially be developed as a new therapy for Stargardt disease, for which there is currently no treat
100     The presence of 2 distinct phenotypes of Stargardt disease (foveal sparing and foveal atrophy) su
101 several inherited visual diseases, including Stargardt disease, fundus flavimaculatus, cone-rod dystr
102        It also provided a molecular basis of Stargardt disease involving this mutation.
103                                              Stargardt disease is a currently untreatable, inherited
104                                              Stargardt disease is a juvenile onset retinal degenerati
105                                  Importance: Stargardt disease is a phenotypically diverse macular dy
106                                   Late-onset Stargardt disease is a subtype of Stargardt disease type
107                                              Stargardt disease is the most common form of early onset
108 resence of choroidal hyperreflective foci in Stargardt disease is, to our knowledge, a potentially ne
109 hough lipofuscin is considered a hallmark of Stargardt disease, its mechanism of formation and its ro
110 ared with their presence in subjects without Stargardt disease (Kruskal-Wallis P < 0.0001 for each va
111 levant information regarding the severity of Stargardt disease, likelihood of central scotoma expansi
112 port also highlights that milder, late-onset Stargardt disease may be confused with AMD.
113 zed primary RPE and the pigmented Abca4(-/-) Stargardt disease mouse model, we provide evidence for t
114  vascular layers of the choroid in eyes with Stargardt disease on SD OCT.
115                                Patients with Stargardt disease or cone-rod dystrophy and disease-caus
116                                Patients with Stargardt disease or cone-rod dystrophy and known or sus
117 nds that could modify the natural history of Stargardt disease or other retinopathies associated with
118 ients with age-related macular degeneration, Stargardt disease, or for quantitative analysis of AF si
119 maculopathy, whose sister was diagnosed with Stargardt disease previously at another centre, was foun
120 y of the Progression of Atrophy Secondary to Stargardt Disease (ProgStar) study.
121 spective Progression of Atrophy Secondary to Stargardt Disease (ProgStar, NCT01977846) study were ana
122 ent study, choroidal hyperreflective foci in Stargardt disease, prominent at the Bruch membrane/RPE c
123                           Five patients with Stargardt disease protected 1 eye from light exposure by
124 hese granules in Abca4(-/-) mice (a model of Stargardt disease) relative to age-matched wild-type (WT
125 incurable blinding retinal diseases, such as Stargardt disease, retinitis pigmentosa (RP), and atroph
126 linked to prevalent retinal diseases such as Stargardt disease, rod-cone dystrophies, and age-related
127 40 eyes), cone-rod dystrophy (CRD, 12 eyes), Stargardt disease (SD, 28 eyes), late-onset SD (LO-SD, 3
128 luorescence (UWF-FAF) in patients with ABCA4 Stargardt disease (STGD) and correlate these data with f
129                                              Stargardt disease (STGD) is a juvenile-onset macular dys
130                                              Stargardt disease (STGD) is the major form of inherited
131                                              Stargardt disease (STGD) is the most common hereditary m
132 ter, are responsible for autosomal recessive Stargardt disease (STGD), an early onset macular degener
133 cessively inherited retinopathies, including Stargardt disease (STGD), cone-rod dystrophy and retinit
134 been associated with the autosomal recessive Stargardt disease (STGD), retinitis pigmentosa (RP19), a
135 lium (RPE), and the choriocapillaris (CC) in Stargardt disease (STGD).
136  caused by mutations in large genes, such as Stargardt disease (STGD).
137  that mutations in the ABCR gene can lead to Stargardt disease (STGD)/fundus flavimaculatus (FFM), au
138                                              Stargardt disease (STGD, also known as fundus flavimacul
139            The high allelic heterogeneity in Stargardt disease (STGD1) complicates the design of inte
140 gle-copy variants of the autosomal recessive Stargardt disease (STGD1) gene ABCR (ABCA4) have been sh
141                                    Recessive Stargardt disease (STGD1) is an inherited juvenile macul
142                                              Stargardt disease (STGD1) is characterized by macular at
143 with molecularly-confirmed, ABCA4-associated Stargardt disease (STGD1) relative to normal controls.
144 ansporter (ABCA4) protein that is mutated in Stargardt disease (STGD1), a juvenile macular dystrophy.
145 atients present with a clinical diagnosis of Stargardt disease (STGD1), a recessive form of macular d
146 nction mutations in ABCA4 are known to cause Stargardt disease (STGD1), an inherited retinal degenera
147 ent-naive eyes with geographic atrophy (GA), Stargardt disease (STGD1), Best disease, pseudoxanthoma
148                                              Stargardt disease (STGD1), known as inherited retinal dy
149 at exceed single AAV cargo capacity, such as Stargardt disease (STGD1), the most common inherited mac
150 leted for 150 families segregating recessive Stargardt disease (STGD1).
151 to the diagnosis and monitoring of recessive Stargardt disease (STGD1).
152 f the natural history of autosomal recessive Stargardt disease (STGD1).
153 e best known of which is autosomal recessive Stargardt disease (STGD1).
154  risk factors for BCVA loss in patients with Stargardt disease (STGD1).
155                          Autosomal recessive Stargardt disease (STGD1, MIM 248200) is caused by mutat
156  implicated in an autosomal dominant form of Stargardt disease (STGD3), a type of juvenile macular de
157  lesions in the retrospective Progression of Stargardt Disease study.
158                                              Stargardt disease, the most common inherited macular dys
159 h was performed to identify SD-OCT images in Stargardt disease; these findings were reviewed for the
160 atients with retinal phenotypes ranging from Stargardt disease to retinitis pigmentosa.
161 ew outcome measures for treatment trials for Stargardt disease type 1 (STGD1) and other macular disea
162                                              Stargardt disease type 1 (STGD1) is a genetic disorder t
163 Late-onset Stargardt disease is a subtype of Stargardt disease type 1 (STGD1), defined by an age of o
164 ay can induce retinal toxicity, as occurs in Stargardt disease type 1 (STGD1).
165 ts with a genetically confirmed diagnosis of Stargardt disease type 1 and >=2 visual acuity measureme
166                     Visual acuity decline in Stargardt disease type 1 follows a nonlinear course, var
167 uate the efficacy of emerging treatments for Stargardt disease type 1 in clinical trials.
168                                              Stargardt disease type 1 patients (carrying at least 1 m
169                                           In Stargardt disease type 1, macular sensitivity declines s
170 te subfamily A member 4, are responsible for Stargardts Disease type 1 (STGD1), the most common form
171 patients, median age at initial diagnosis of Stargardt disease was 9.5 years, and the median duration
172                                 Diagnosis of Stargardt disease was based on ophthalmic history and co
173 lary retina of an eye donor with ungenotyped Stargardt disease was examined microscopically.
174                       Using a mouse model of Stargardt disease, we found that pharmacological interve
175                Here, using a murine model of Stargardt disease, we show that the propensity of vitami
176  of 13 patients with a clinical diagnosis of Stargardt disease were evaluated in a retrospective case
177 707 macular SD-OCT scans of 13 patients with Stargardt disease were reviewed and evaluated for the pr
178 regularly shaped in 26 of 41 eyes (64%) with Stargardt disease when compared to 0 of 30 healthy eyes
179 ness were significantly reduced in eyes with Stargardt disease when compared to healthy eyes (272.8 +
180 were significantly enriched in patients with Stargardt disease when compared with their presence in s
181 cated that female sex might be a modifier in Stargardt disease, which is an ABCA4-associated retinopa
182              One hundred fifty patients with Stargardt disease who were examined at least four times
183                                           In Stargardt disease with DDAF lesions, fundus autofluoresc
184 ewed for patients with genetically confirmed Stargardt disease with peripheral pigmented retinal lesi
185 rmore, chronic treatment of a mouse model of Stargardt disease with the RPE65 antagonists abolishes t
186 h macular dystrophy, originally diagnosed as Stargardt disease, with a significantly variable age at

 
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