ライフサイエンスコーパス: AMD

1 AMD continues to remain a significant public health prob

2 AMD participants had better-eye visual acuity (VA) <20/3

3 AMD was associated with ever use of organochlorine [OR=2

4 AMD was diagnosed based on fundus photographs using the

5 f aflibercept increased (1.1 injections/1000 AMD patients in 2011 to 183.0 injections/1000 in 2015).

6 fter (in 2006, 58.8 and 35.3 injections/1000 AMD patients, respectively; in 2015, 294.4 and 100.7 inj

7 otyping was performed on a subsample of 1284 AMD cases and controls for 93 single nucleotide polymorp

8 um nutrient levels; and others (total of 139 AMD and non-AMD phenotypes).

9 follow-up median of 4.0 years and among 292 AMD eyes (without advanced disease at baseline) with com

10 52,690 normal macular OCT images and 48,312 AMD macular OCT images were selected.

11 examined all Cochrane reviews that addressed AMD, cataract, DR, and glaucoma; were published as of Ju

12 nine incident intermediate and 1356 advanced AMD cases (primarily neovascular AMD) were confirmed by

13 urrent evidence for EPA and DHA and advanced AMD is discordant, though there was no association with

14 intake of ALA and intermediate and advanced AMD.Seventy-five thousand eight hundred eighty-nine wome

15 nd recommendations for their use in advanced AMD trials.

16 eas pigment changes and features of advanced AMD are less frequent.

17 provide insight into the absence of advanced AMD in nonhuman primates.

18 to a large increase in the risk of advanced AMD in some genotype subgroups.

19 iants in cases with intermediate or advanced AMD was compared with controls.

20 Progression to advanced AMD.

21 ALA intake was not associated with advanced AMD in either time period.

22 hough there was no association with advanced AMD in the present study.

23 evelopment of therapeutic strategies against AMD.

24 Amiodarone (AMD) and nifekalant (NIF) are used in the treatment of v

25 as 2 out of 16 confirmed associations in an AMD candidate SNP analysis were filtered, representing a

26 ted macular degeneration (AMD) risk loci and AMD sub-phenotypes.

27 Normal and AMD patients who had a macular OCT.

28 Any AMD, early AMD, intermediate AMD, and late AMD graded ac

29 th healthy controls (P < 0.001) and atrophic AMD patients (P < 0.001).

30 ith exudative AMD, 46 patients with atrophic AMD and 111 healthy controls.

31 to 3.06; P = .72), psychosocial well-being (AMD, -0.59; 95% CI, -3.92 to 2.74; P = .73), and sexual

32 92 to 2.74; P = .73), and sexual well-being (AMD, -2.94; 95% CI, -7.01 to 1.12; P = .15) 2 years post

33 rvival (OR: 1.25, 95% CI: 0.67-2.31) between AMD- and NIF-treated patients.

34 sion models examined the association between AMD and VSF in the 3 ethnic groups, adjusting for age, s

35 in the prevalence of VMA in eyes affected by AMD compared with age-matched controls and no difference

36 ononuclear phagocytes (MP) that characterize AMD and showed accelerated resolution of inflammation.

37 Age-related macular degeneration (AMD) affects millions of people throughout the world.

38 Age-related macular degeneration (AMD) affects the retinal pigment epithelium (RPE), a cel

39 eovascular age-related macular degeneration (AMD) among Medicare beneficiaries.

40 condary to age-related macular degeneration (AMD) and 2 eyes (5%) had geographic atrophy secondary to

41 coincident age-related macular degeneration (AMD) and 2 with myopic macular degeneration.

42 Age-related macular degeneration (AMD) and related macular dystrophies (MDs) are a major c

43 eovascular age-related macular degeneration (AMD) and to demonstrate its use to model the impact of s

44 eovascular age-related macular degeneration (AMD) and to provide recommendations on the use of these

45 on between age-related macular degeneration (AMD) and vision-specific functioning (VSF).

46 developing age-related macular degeneration (AMD) continued for people born during the Baby Boom year

47 ation with age-related macular degeneration (AMD) have been described.

48 y and late age-related macular degeneration (AMD) in a Singaporean Malay population and to validate t

49 exudative age-related macular degeneration (AMD) in comparison with eyes with nonexudative AMD and a

50 valence of age-related macular degeneration (AMD) in countries ranging from Southern to Northern Euro

51 iate-stage age-related macular degeneration (AMD) in patients with acquired immunodeficiency syndrome

52 Age-related macular degeneration (AMD) is a leading cause of irreversible blindness among

53 Age-related macular degeneration (AMD) is a major cause of visual impairment that affects

54 Age-related macular degeneration (AMD) is a progressive retinal neurodegenerative disorder

55 Age-related macular degeneration (AMD) is the leading cause of irreversible vision impairm

56 Age-related macular degeneration (AMD) is the most common cause of blindness for individua

57 impact of age-related macular degeneration (AMD) on short out-loud and sustained silent reading spee

58 eovascular age-related macular degeneration (AMD) or fellow control eyes, as well as analyze risk fac

59 eyes with age-related macular degeneration (AMD) receiving anti-vascular endothelial growth factor (

60 y (DR) and age-related macular degeneration (AMD) remains unclear.

61 nts within age-related macular degeneration (AMD) risk loci and AMD sub-phenotypes.

62 ctions and age-related macular degeneration (AMD) risk.

63 a range of age-related macular degeneration (AMD) severity are associated with their performance on f

64 ed form of age-related macular degeneration (AMD) that leads to progressive and irreversible loss of

65 eovascular age-related macular degeneration (AMD) treated initially with bevacizumab and subsequently

66 ients with age-related macular degeneration (AMD) using mass spectrometry (MS).

67 ) cells in age-related macular degeneration (AMD) using polarimetry.

68 ients with age-related macular degeneration (AMD) who are being considered for treatment with antioxi

69 pants with age-related macular degeneration (AMD) with bilateral large drusen or noncentral GA and at

70 arities to age-related macular degeneration (AMD), a common and genetically complex disorder, which c

71 Age-related macular degeneration (AMD), a leading contributor of vision loss, currently la

72 Age-related macular degeneration (AMD), a multifactorial disease with variable phenotypic

73 s, such as age-related macular degeneration (AMD), develop late in life and are considered to be of c

74 including age-related macular degeneration (AMD), glaucoma and refractive error.

75 In age-related macular degeneration (AMD), rare variants in the complement system have been d

76 termediate age-related macular degeneration (AMD), without other vitreoretinal pathology.

77 he risk of age-related macular degeneration (AMD).

78 termediate age-related macular degeneration (AMD).

79 cidence of age-related macular degeneration (AMD).

80 llmarks of age-related macular degeneration (AMD).

81 genesis of age-related macular degeneration (AMD).

82 with late age-related macular degeneration (AMD).

83 stages of age-related macular degeneration (AMD).

84 eovascular age-related macular degeneration (AMD).

85 stress in Age-related macular degeneration (AMD).

86 ients with Age-related Macular Degeneration (AMD).

87 setting of age-related macular degeneration (AMD).

88 exudative age-related macular degeneration (AMD).

89 rs such as age-related macular degeneration (AMD).

90 sed state (age related macular degeneration, AMD) in the retina.

91 819 participants were at risk for developing AMD based on fundus images obtained at baseline visits.

92 ntributed to an increased risk of developing AMD (odds ratio, 2.04; 95% CI, 1.47-2.82; P < .001).

93 cells (hiPSCs) from patients with diagnosed AMD, including two donors with the rare ARMS2/HTRA1 homo

94 is the primary cause of acid mine drainage (AMD).

95 For all early AMD (grade 1-3), there was no relationship with MDS (P t

96 Any AMD, early AMD, intermediate AMD, and late AMD graded according to

97 Two individuals with baseline early AMD from the 142 at risk had developed late AMD at follo

98 4909 (49.3%) were male; 590 (5.9%) had early AMD (241 Chinese, 161 Malays, and 188 Indians) and 60 (0

99 le; 2137 had no signs of AMD, 2209 had early AMD, and 150 had late AMD, of whom 104 had nvAMD.

100 Patients with either drusen or RPD in early AMD underwent OCTA imaging of the superior, inferior, an

101 000 estimated new cases of AMD, mainly early AMD, will develop every year in individuals 50 years or

102 Prevalence of early AMD increased from 3.5% (95% confidence interval [CI] 2.

103 The weighted prevalence of early AMD was 14.8% (95% CI, 11.7%-18.6%) and of intermediate

104 hanges representing characteristics of early AMD, providing a valuable model for investigating the ro

105 e number of individuals in Europe with early AMD will range between 14.9 and 21.5 million, and for la

106 rrection, no SNPs were associated with early AMD, late AMD, or nvAMD.

107 time was found in eyes affected by exudative AMD.

108 For discriminating exudative AMD patients, the optimum diagnostic cutoff of DKK-1 was

109 The incidence of RVMA in exudative AMD eyes was significantly lower compared with nonexudat

110 hat DKK-1 levels were decreased in exudative AMD patients, compared with healthy controls (P < 0.001)

111 The odds ratio (OR) of exudative AMD was 11.71 (95% CI; 5.24-6.13) for lowest versus uppe

112 as obtained from 128 patients with exudative AMD, 46 patients with atrophic AMD and 111 healthy contr

113 s present in 101 (25.1%) eyes with exudative AMD, 84 (24.0%) eyes with nonexudative AMD, and 84 (26.8

114 For AMD eyes with large drusen and no advanced disease, we b

115 ranging from 19 of 107 outcomes (17.8%) (for AMD) to 24 of 89 outcomes (27.0%) (for glaucoma).

116 llion dollars per year are spent on care for AMD patients in the US.

117 nalysis the only significant risk factor for AMD in LSOCA was smoking; the relative risk vs never-smo

118 HDL-cholesterol is a causal risk factor for AMD risk and that increasing HDL-cholesterol (particular

119 d ABCA1) were identified as risk factors for AMD, although how cholesterol efflux influences accumula

120 esticides may be modifiable risk factors for AMD.

121 erent conditions simulating risk factors for AMD.

122 Fundus images were graded for AMD using the Wisconsin Age-related Maculopathy Grading

123 However, the preferred practice patterns for AMD recommend identifying individuals with this stage of

124 scovery cohort) had detailed phenotyping for AMD; other eye conditions; cardiovascular, neurologic, g

125 Use of bevacizumab and ranibizumab for AMD plateaued as of 2011/2012 and decreased thereafter (

126 ue for determining the magnitude of risk for AMD at the genetic level, one will need to examine the r

127 To determine whether the 5-year risk for AMD declined by generation and to identify factors that

128 of the 2900 individuals (50.1%) at risk for AMD were followed up after 6 years (mean [SD] age, 60.7

129 suggest that lipids have a greater role for AMD compared with Alzheimer's disease, but a lesser role

130 mination, color fundus photography (used for AMD staging), and spectral-domain OCT (to evaluate the p

131 n Influence on Macula of Persons Issued From AMD Parents [LIMPIA]) with a 6-month treatment period, f

132 Further, AMD risk genes participate in multiple networks with int

133 t with their medical record; 320 (24.8%) had AMD despite no diagnosis of AMD in the medical record.

134 al of 30.0% of eyes with undiagnosed AMD had AMD with large drusen that would have been treatable wit

135 ongitudinal studies of peripheral changes in AMD and their impact on visual function may contribute t

136 Correlations appear to be more complex in AMD and RVO.

137 pro re nata (PRN) dosing were correlated in AMD (r = -0.27) and RVO (r = -0.72) trials, but not in D

138 Multiple RPE fates in AMD, including intraretinal cells that are highly progno

139 preserved photoreceptor layers are found in AMD.

140 lete representation of changes that occur in AMD than can be detected using color fundus photography

141 s current understanding of GA progression in AMD and the factors known or postulated to be relevant t

142 rstand the etiology of Abeta proteostasis in AMD, we delivered recombinant adeno-associated virus (AA

143 atomic end points and response to therapy in AMD clinical trials.

144 may manifest other macular disease including AMD and myopic macular degeneration.

145 ticularly via CETP inhibition) will increase AMD risk.

146 Any AMD, early AMD, intermediate AMD, and late AMD graded according to the Beckman clinic

147 e multivariable-adjusted HR for intermediate AMD comparing ALA intake at the top quintile to the bott

148 For intermediate AMD, the pooled hazard ratio (HR) between the 2 cohorts

149 iated with an increased risk of intermediate AMD before 2002 but not afterward.

150 8% (95% CI, 11.7%-18.6%) and of intermediate AMD was 10.5% (95% CI, 8.3%-13.1%) among nonindigenous A

151 ollected data from 68 eyes with intermediate AMD from 68 patients with spectral-domain optical cohere

152 In subjects with intermediate AMD, choroidal thickness and vessel volume are reduced i

153 Late AMD was found in 0.96% (95% CI, 0.59%-1.55%) of nonindig

154 no SNPs were associated with early AMD, late AMD, or nvAMD.

155 y AMD, early AMD, intermediate AMD, and late AMD graded according to the Beckman clinical classificat

156 determined the prevalence of early and late AMD in Europe from 1990 to 2013 using the European Eye E

157 associated with lower odds of early and late AMD in white populations.

158 en physical activity and both early and late AMD using random-effects meta-analysis.

159 ge-standardized incidences of early and late AMD were 5.89% (95% confidence interval [CI], 4.81-7.16)

160 Prevalence of early and late AMD, BCVA, and number of AMD cases.

161 Incidence of early and late AMD.

162 sual acuity (BCVA) was compared between late AMD subtypes; geographic atrophy (GA) and choroidal neov

163 AMD from the 142 at risk had developed late AMD at follow-up, with a 6-year cumulative incidence of

164 between 14.9 and 21.5 million, and for late AMD between 3.9 and 4.8 million.

165 gender across all age groups except for late AMD in the oldest age category, and a trend was found sh

166 %-21.5%) in those aged >/=85 years; for late AMD these figures were 0.1% (95% CI 0.04%-0.3%) and 9.8%

167 ays, and 188 Indians) and 60 (0.6%) had late AMD (25 Chinese, 21 Malays, and 14 Indians).

168 of AMD, 2209 had early AMD, and 150 had late AMD, of whom 104 had nvAMD.

169 ale is useful in predicting the risk of late AMD development in Asians.

170 The incidence of late AMD in our population was similar to that of the Beaver

171 llow-up and wide CIs for progression to late AMD limit definitive conclusions from these findings.

172 incidence of progression from early to late AMD of 24.5 per 1000 persons (95% CI, 5.0-111.7 per 1000

173 of single-nucleotide polymorphisms with late AMD adjusted for age and sex.

174 In the Malay group, those with late AMD had a 13.5% drop in VSF (beta = -0.49; 95% CI, -1.01

175 Moreover, Chinese participants with late AMD had a clinically significant 19.1% loss of VSF (beta

176 terranean dietary pattern in those with late AMD, although it does not support previous reports of a

177 Among the 1727 patients with late AMD, the mean (SD) age was 78.7 (7.4) years, and 668 (38

178 CRP concentrations are associated with late AMD.

179 e studies in non-neovascular and neovascular AMD was held.

180 lial growth factor therapies for neovascular AMD had decreased mortality compared with those who did

181 t first received ranibizumab for neovascular AMD was 35%, and varied significantly (0.9%-84.6%) acros

182 Twelve eyes (32%) had neovascular AMD and 1 eye (3%) had neovascularization secondary to p

183 macular degeneration 4 included neovascular AMD (nvAMD) and geographic atrophy (GA).

184 received ranibizumab for initial neovascular AMD treatment in 2009 vs 2006.

185 ty patients with treatment-naive neovascular AMD in 1 eye randomized 1:2 to monthly or TREX ranibizum

186 atment-naive CNV due to AMD, non-neovascular AMD, and normal controls.

187 s with MPNs had a higher risk of neovascular AMD (adjusted HR, 1.4; 95% CI, 1.2-1.6).

188 dministered for the treatment of neovascular AMD.

189 56 advanced AMD cases (primarily neovascular AMD) were confirmed by medical record review.The multiva

190 geographic atrophy/fibrotic scar/neovascular AMD in the fellow eye.

191 lial (RPE) hemorrhage related to neovascular AMD (odds ratio 1.55 [95% confidence interval 1.31-1.84]

192 onditioning on participants with neovascular AMD (P = 2.42 x 10(-4)).

193 ration offspring of parents with neovascular AMD in the LIMPIA trial, MPOD as measured with the modif

194 For studies in patients with neovascular AMD, increased need for visualization of the vasculature

195 1400 OCT scans of patients with neovascular AMD.

196 ration offspring of parents with neovascular AMD.

197 g anatomical effect in eyes with neovascular AMD.

198 A total of 968 eyes (75.2%) had no AMD, in agreement with their medical record; 320 (24.8%)

199 levels; and others (total of 139 AMD and non-AMD phenotypes).

200 One eye from a 75-year-old nonexudative AMD patient with GA was quantitatively analyzed.

201 D) in comparison with eyes with nonexudative AMD and age-matched controls, and to evaluate prospectiv

202 Patients with nonexudative AMD were prospectively enrolled in an SS-OCT imaging stu

203 ative AMD, 84 (24.0%) eyes with nonexudative AMD, and 84 (26.8%) eyes with no signs of AMD (no statis

204 deep learning-based automated assessment of AMD from fundus images can produce results that are simi

205 t of plasma-based metabolomics biomarkers of AMD, and to identify novel targets for treatment of this

206 nya, more than 100000 estimated new cases of AMD, mainly early AMD, will develop every year in indivi

207 lement pathway modify the clinical course of AMD and increase the risk of developing specific sub-phe

208 320 (24.8%) had AMD despite no diagnosis of AMD in the medical record.

209 Currently, knowledge of the epidemiology of AMD in Australia remains scarce because of a paucity of

210 major retinal pathophysiological features of AMD and will be instrumental in mechanistic understandin

211 Except for positive family history of AMD with rs3750846, all genotype-phenotype associations

212 uorescein angiography, and family history of AMD.

213 The incidence of AMD in LSOCA was compared with that in the Multi-Ethnic

214 Incidence of AMD recorded in specialized hospital-based care.

215 he 5-year age- and sex-adjusted incidence of AMD was 8.8% in the Greatest Generation (born during 190

216 t human graders in the current management of AMD and could address the costs of screening or monitori

217 Here, we used murine models of AMD to examine the contribution of CFH to disease etiolo

218 e of early and late AMD, BCVA, and number of AMD cases.

219 Using a panel of AMD biomarkers and candidate drug screening, combined wi

220 Presence of AMD as defined by the Clinical Age-Related Maculopathy S

221 We observed a decreasing prevalence of AMD and an improvement in visual acuity in CNV occuring

222 at address the development or progression of AMD.

223 activity on the onset and/or progression of AMD.

224 Projections of AMD showed an almost doubling of affected persons despit

225 s older than 50 years of age with a range of AMD severity.

226 the race/ethnicity- and sex-adjusted risk of AMD in LSOCA was 1.75 (95% CI 1.16, 2.64; P = .008), des

227 f AMD in patients with MPNs with the risk of AMD in matched controls from the general population.

228 To compare the risk of AMD in patients with MPNs with the risk of AMD in matche

229 The rates and absolute risk of AMD were calculated.

230 ia for OCT-defined atrophy in the setting of AMD has been proposed based on an international consensu

231 ve AMD, and 84 (26.8%) eyes with no signs of AMD (no statistical difference was found; P = 0.3384).

232 icant, with respect to eyes with no signs of AMD (P = 0.1013).

233 rovided a blood sample; 2137 had no signs of AMD, 2209 had early AMD, and 150 had late AMD, of whom 1

234 ical pathways underlying different stages of AMD.

235 he potential to improve our understanding of AMD pathogenesis, to support the development of plasma-b

236 %], and 159 other [12.4%]); 1282 had data on AMD status at follow-up.

237 ned to categorize images as either normal or AMD.

238 nges from baseline in BCVA and CRT in pooled AMD trial data.

239 who meet criteria for supplements to prevent AMD progression should be offered zinc and antioxidants

240 In age-adjusted regressions, AMD participants, compared to controls, read 46 words pe

241 ble analyses of the LLQ scores and age, RIT, AMD severity, subfoveal choroidal thickness [SFCT], phak

242 cohort reported similar breast satisfaction (AMD, -0.68; 95% CI, -4.42 to 3.06; P = .72), psychosocia

243 The hiPSC-derived RPE cells produce several AMD/drusen-related proteins, and those from the AMD dono

244 tional hazards models adjusted for age, sex, AMD severity, VA, history of cataract surgery, and assig

245 e associated with both early- and late-stage AMD, but others were associated with only one stage.

246 rdam staging system into 5 exclusive stages (AMD 0-4) and a separate category of large drusen (>/=125

247 ) populated the actomyosin.ADP closed state (AMD(C)) 5-fold more than the actomyosin.ADP open state (

248 old more than the actomyosin.ADP open state (AMD(O)) and to a greater degree than MYO1C(C) and MYO1C(

249 As such, AMD represents a significant and important clinical prob

250 The AMD-associated CFH(H402) variant markedly increased this

251 /drusen-related proteins, and those from the AMD donors show significantly increased complement and i

252 , both groups read at similar speeds, though AMD patients demonstrated substantially lower comprehens

253 Thus AMD most likely represents an endophenotype with differi

254 ncluded eyes with treatment-naive CNV due to AMD, non-neovascular AMD, and normal controls.

255 triggered by pathologic stimuli relevant to AMD, such as cholesterol crystals and ox-LDL.

256 on OCT was proposed for atrophy secondary to AMD.

257 wed that, compared to the control treatment, AMD did not improve short-term survival (odds ratio (OR)

258 ual function may contribute to understanding AMD pathogenesis.

259 Prevalence of undiagnosed AMD was not different for ophthalmologists and optometri

260 A total of 30.0% of eyes with undiagnosed AMD had AMD with large drusen that would have been treat

261 Among eyes with undiagnosed AMD, 32 (10.0%) had hyperpigmentation, 43 (13.4%) had hy

262 c as opposed to complex retinopathies, using AMD as an example of the latter.

263 We evaluated 155 eyes at various AMD stages.

264 raretinal RPE migrations occurred in various AMD stages, and that they occurred more commonly in eyes

265 ased on prespecified criteria for active wet AMD.

266 cts with advanced, treatment-experienced wet AMD were randomly assigned (3:1) to treatment and non-ge

267 Eligible subjects were >/=65 years, had wet AMD, and had best-corrected visual acuity (BCVA) 10/200

268 tory data analysis suggests stability of wet AMD over the 36-month period.

269 erse effects of therapy in patients with wet AMD and PDR.

270 long-term mortality in individuals with wet AMD treated with bevacizumab compared to a same age and

271 d to a same age and gender group without wet AMD.

272 ions are widely used in the treatment of wet-AMD and PDR.

273 ed States, yet little is known about whether AMD is appropriately diagnosed in primary eye care.

274 While AMD histopathology involves retinal pigment epithelium (

275 photographs were graded using the Wisconsin AMD grading system.

276 96 million individuals will be affected with AMD.

277 ific pesticides consistently associated with AMD included chlordane, dichlorodiphenyltrichloroethane

278 fied novel loci and pathways associated with AMD risk, which has provided an excellent platform for a

279 nt risk variants known to be associated with AMD.

280 s were used to compute the associations with AMD outcomes.

281 gnificance, and test their associations with AMD.

282 Drusen are seen in a majority of eyes with AMD in both the mid and far periphery, whereas pigment c

283 inal changes are more prevalent in eyes with AMD than in control eyes.

284 multimodal imaging for a series of eyes with AMD, and reviewed the results of this analysis to define

285 ffected (n = 60) members of 22 families with AMD and a case-control cohort consisting of 1831 unrelat

286 iants in the CFH, CFI, C9, and C3 genes with AMD, serum levels of corresponding proteins, and C3b deg

287 l of 484 (951 eyes) AREDS2 participants with AMD (cases) and 89 (163 eyes) controls without AMD had g

288 Participants with AMD have altered plasma metabolomic profiles compared wi

289 ociations of rare pLoF variant pathways with AMD sub-phenotypes were analyzed using logistic and line

290 t consisting of 1831 unrelated patients with AMD and 1367 control individuals from the European Genet

291 alyses included 100 eyes of 51 patients with AMD carrying a CFH variant (mean [SD] age, 66.7 [12.1] y

292 henotypical characteristics of patients with AMD carrying a rare variant in the CFH gene.

293 Home telemonitoring of patients with AMD for early detection of CNV vs usual care.

294 The 1831 unrelated patients with AMD had a mean (SD) age of 75.0 (9.4) years, and 60.5% w

295 lement-inhibiting therapy than patients with AMD in general.

296 ristics of 194 treatment-naive patients with AMD treated with as-needed ranibizumab for at least 2 ye

297 Home telemonitoring of patients with AMD who are at risk for CNV was cost-effective compared

298 OCT images in a population of patients with AMD.

299 te, native-English speakers with and without AMD.

300 D (cases) and 89 (163 eyes) controls without AMD had gradable color and FAF images.

301 07) compared with their counterparts without AMD.