ライフサイエンスコーパス: AMD

1 AMD discharges offer generally high sulfate concentratio

2 AMD makes reading challenging and inefficient.

3 AMD was associated with less anxiety (OR 0.67; CI 95% 0.

4 AMD was not associated with depression (OR 0.93; CI 95%

5 AMD was not associated with depression.

6 AMD, defined according to the Beckman Initiative for Mac

7 AMD- and non-AMD participants had a similar prevalence a

8 (SNPs), coding and splice-site regions of 10 AMD-(related) genes (ARMS2, C3, C9, CD46, CFB, CFH, CFI,

9 A total of 364 patients (165 AMD and 199 PCV) were included.

10 The effect of 52 AMD-associated genetic variants on the identified metabo

11 Of 52 AMD-associated genetic variants, 7 variants were associa

12 ive clinical trial dataset that includes 671 AMD fellow eyes with 13,954 observations before any sign

13 h nonexudative (54.2%) and exudative (45.8%) AMD to measure retinal vessel density (VD) from the supe

14 drusen-like pathologies, as well as advanced AMD-like pathologies.

15 ce in standard ETDRS VA between non-advanced AMD (0.06 +/- 0.02 logMAR) and normal groups (0.04 +/- 0

16 was significantly worse in the non-advanced AMD group compared to normals (0.67 +/- 0.07 in AMD; 0.4

17 tion tests were performed on 23 non-advanced AMD subjects (AREDS grade 1-4 on simplified scale) and 3

18 Non-advanced AMD subjects also had significantly worse reading perfor

19 to detect visual dysfunction in non-advanced AMD.

20 stimate the cumulative incidence of advanced AMD for the high-risk groups, especially in ALIENOR.

21 eviously suggested as a new form of advanced AMD, and herein replicated.

22 n increased risk for progression to advanced AMD, whereas diabetes and glaucoma were associated with

23 may prevent or delay progression to advanced AMD.

24 ual dysfunction, especially delayed RMDA, an AMD risk indicator assessing efficiency of retinoid resu

25 retinopathy with macular oedema (15.8%), and AMD (11.0%).

26 acrophage function as a factor in aging- and AMD-associated pathology.

27 adjusting for age, gender, baseline BCVA and AMD subtype, A (protective) allele of C2-CFB-SKIV2L rs42

28 studying the link between oral infection and AMD pathogenesis in individuals with periodontitis.

29 The prevalence of any AMD, early AMD, intermediate AMD, or late AMD, geographi

30 tering variants in candidate target genes at AMD-associated loci.

31 dels for progression to late AMD or atrophic AMD were only developed (each including age) based on: (

32 potential new therapeutic strategy to combat AMD.

33 idal neovascularization (CNV) can complicate AMD and lead to severe visual acuity reduction.

34 condary to age-related macular degeneration (AMD) and best-corrected visual acuity (BCVA) of 20/80 to

35 ed risk of age-related macular degeneration (AMD) and disease progression, but the precise biological

36 jects with age-related macular degeneration (AMD) and its association with AMD in a large European co

37 lopment of age-related macular degeneration (AMD) and other complementopathies.

38 r advanced age-related macular degeneration (AMD) are based on a restrictive set of risk factors.

39 A nor late age-related macular degeneration (AMD) at baseline were included.

40 rusen from age-related macular degeneration (AMD) before and after the drusen spontaneously resolved

41 to active age-related macular degeneration (AMD) disease progression in both eyes.

42 nt(s) with age-related macular degeneration (AMD) have a 45% lifetime risk of developing the disease.

43 Age-related macular degeneration (AMD) is a chronic eye condition that leads to permanent

44 Age-related macular degeneration (AMD) is a chronic, multifactorial disorder and a leading

45 Age-related macular degeneration (AMD) is a common multifactorial disease in the elderly w

46 eovascular age-related macular degeneration (AMD) is a highly effective advance in the retinal arment

47 Age-related macular degeneration (AMD) is the leading cause of legal blindness in adults 6

48 eovascular age-related macular degeneration (AMD) that had type 1 macular neovascularization (MNV) (9

49 Age-related macular degeneration (AMD), a leading cause of irreversible vision impairment

50 ibutors to age-related macular degeneration (AMD), a leading cause of irreversible vision loss worldw

51 tiology of age-related macular degeneration (AMD), a major cause of blindness in the elderly.

52 a (RP) and age-related macular degeneration (AMD), are among the leading causes of incurable blindnes

53 other than age-related macular degeneration (AMD), diabetic retinopathy, glaucoma, or cornea guttata

54 nexudative age-related macular degeneration (AMD), exudative AMD, hereditary maculopathy, and toxic m

55 on loss in age-related macular degeneration (AMD), it is critical to detect retinal dysfunction befor

56 genesis of age-related macular degeneration (AMD), the leading cause of irreversible blindness in the

57 iated with age-related macular degeneration (AMD), the most common cause of incurable vision loss in

58 genesis of age-related macular degeneration (AMD), the role of retinal perfusion is unclear.

59 er, showed age-related macular degeneration (AMD)-like fundus changes.

60 y for late age-related macular degeneration (AMD).

61 ffected by age-related macular degeneration (AMD).

62 condary to age-related macular degeneration (AMD).

63 duals with age-related macular degeneration (AMD).

64 SS-OCT) in age-related macular degeneration (AMD).

65 eovascular age-related macular degeneration (AMD).

66 ndition in age-related macular degeneration (AMD).

67 including age-related macular degeneration (AMD).

68 ase(PD) to age-related macular degeneration (AMD).

69 as well as age-related macular degeneration (AMD).

70 o advanced age-related macular degeneration (AMD).

71 nts associated with Chr1- and Chr10-directed AMD.

72 Mixing of acid mine drainage (AMD) and hydraulic fracturing flowback fluids (HFFF) cou

73 Acid mine drainage (AMD) is the most significant environmental pollution pro

74 be especially important as a therapy for dry AMD patients who have another common age-related comorbi

75 mages from 97 patients/eyes with GA with dry AMD were collected retrospectively from existing anonymi

76 of patients with wet AMD, patients with dry AMD, and in age-matched individuals without AMD as contr

77 Among the 97 eyes with dry AMD, the mean GA area was 7.62 +/- 7.77 mm(2) from FAF i

78 nical trials for therapies targeting earlier AMD stages than GA expansion.

79 The prevalence of any AMD, early AMD, intermediate AMD, or late AMD, geographic atrophy,

80 re-function relationships in aging and early AMD gained from ALSTAR2, especially the critical transit

81 eatments and prevention strategies for early AMD is a limited understanding of the temporal interrela

82 nally valid, structural biomarkers for early AMD, suitable for use in forthcoming clinical trials as

83 +/- 0.5, and 1.9 +/- 3.4 for healthy, early AMD, and intermediate AMD eyes, respectively).

84 sparse in healthy eyes, infrequent in early AMD eyes, and frequent but highly variable among interme

85 tify and validate robust biomarkers in early AMD stages.

86 with no AMD or aging changes, 11.5% in early AMD, 25.1% in intermediate AMD, and 51.1% in late AMD.

87 and rod-mediated (scotopic) vision in early AMD, including delayed rod-mediated dark adaptation (RMD

88 tation of the retinal layers including early AMD features of RPD and regular drusen separately on SD-

89 Macular Degeneration (ALSTAR2) is that early AMD is a disease of micronutrient deficiency and vascula

90 tics while transitioning from aging to early AMD.

91 ither in normal macular health or with early AMD will be enrolled and followed for 3 years to examine

92 s (ranibizumab or aflibercept) due to either AMD or DME comorbidity, showed a significant reduction o

93 elated macular degeneration (AMD), exudative AMD, hereditary maculopathy, and toxic maculopathy.

94 Among exudative AMD patients with glaucoma or suspected of having glauco

95 e used to compare nonexudative and exudative AMD eyes and the impact of anti-vascular endothelial gro

96 between eyes with nonexudative and exudative AMD using optical coherence tomography angiography (OCT-

97 New-onset investigator-determined exudative AMD was reported more frequently in pegcetacoplan-treate

98 nts with a diagnosis of unilateral exudative AMD and confirmed to have or suspected of having glaucom

99 w eyes of patients with unilateral exudative AMD ranged from 6.25% to 27%.

100 culopathy in patients with IC were exudative AMD (1.5%), drusen (0.8%), nonexudative AMD (0.3%), toxi

101 tinal VD is decreased in eyes with exudative AMD compared with nonexudative AMD but is unaffected by

102 A total of 234 patients with exudative AMD were initially treated with 3 monthly IAI and therea

103 In eyes with exudative AMD, previous anti-VEGF treatments did not impact retina

104 fewer (adjusted odds ratio, 3.8 and 10.6 for AMD and PCV, respectively).

105 in the mining and consulting businesses for AMD prediction, and any improvements in its efficiency,

106 These tests show promise as endpoints for AMD studies.

107 mum angle of resolution (logMAR) letters for AMD and PCV patients, respectively.

108 the way toward making precision medicine for AMD patients a reality in the near future.

109 ulation from Russia, a higher prevalence for AMD was associated mainly with older age, rural region o

110 d natural vision in restoration of sight for AMD patients.

111 ts could be amendable for new treatments for AMD that currently are under development.

112 Four AMD discharges and HFFF from two unconventional Marcellu

113 with an increasing population suffering from AMD and DR, there is an urgent need to develop new thera

114 Higher AMD prevalence was correlated with older age (odds ratio

115 apitulates the epigenetic hallmarks of human AMD.

116 , the detection of this clinically important AMD-associated lesion.

117 group compared to normals (0.67 +/- 0.07 in AMD; 0.45 +/- 0.04 in normals, p = 0.005).

118 ids may point to nutritional deficiencies in AMD.

119 Prevalence of depression in AMD and non-AMD participants was 7.2% and 8.0%, respecti

120 contributing to complement dysregulation in AMD.

121 w that systemic FHR-4 levels are elevated in AMD (P-value = 7.1 x 10(-6)), whereas no difference is s

122 Type 2 MNV remains a rare entity in AMD.

123 The percentage of FMPD in AMD offspring is nearly twice that reported for the gene

124 rare variants in complement pathway genes in AMD.

125 de therapies and/or dietary interventions in AMD.

126 tion, genetic variants, and deep learning in AMD in both the Age-Related Eye Disease Study (AREDS) an

127 ncies for CFB was non significantly lower in AMD group (6.5% vs. 13.1%, AOR = 0.49, CI = 0.23-1.04, P

128 ) was found to be non-significantly lower in AMD patients.

129 assess accompanying factors of type 2 MNV in AMD.

130 ed and annular LAMP-1-positive organelles in AMD RPE.

131 s could contribute to disease progression in AMD.

132 deletion of CFHR3 and CFHR1 is protective in AMD and highlight the importance of genetic variants wit

133 ew opportunities to study the role of PRs in AMD pathogenesis.

134 omplement factor 3 (C3) rs2230199 (R102G) in AMD.

135 nstrate that FHR-4 plays a prominent role in AMD pathogenesis.

136 and the retinal pigment epithelium (RPE) in AMD.

137 ale, exome-wide analysis of rare variants in AMD.

138 ablet with LL 2.0ND (114.55 +/- 11.22 wpm in AMD; 145.17 +/- 9.55 wpm in normals p = 0.049).

139 included number of intravitreal injections (AMD and PCV adjusted odds ratio, 12.1 [P = 0.001] and 12

140 evalence of any AMD, early AMD, intermediate AMD, or late AMD, geographic atrophy, and neovascular AM

141 quent but highly variable among intermediate AMD eyes (mean+/-standard deviation [SD] number per eye,

142 was used in cases of early and intermediate AMD as the base imaging method to identify cases of iROR

143 3.4 for healthy, early AMD, and intermediate AMD eyes, respectively).

144 respectively, in the Proxima B intermediate AMD cohort at month 12.

145 mpared with patients with early/intermediate AMD (P < 0.001) and individuals without AMD (P < 0.001).

146 Study eyes with early/intermediate AMD and a diagnosis of CNV in the fellow eye progressed

147 ients with a diagnosis of early/intermediate AMD were extracted between October 2000 and February 201

148 ndividuals with bilateral early/intermediate AMD, rates of progression to GA or CNV were 2.0 and 3.2

149 (3.02) in Proxima B fellow eye intermediate AMD cohort, respectively.

150 reased risk of progression from intermediate AMD to MMI-defined atrophy.

151 s, 11.5% in early AMD, 25.1% in intermediate AMD, and 51.1% in late AMD.

152 , Chr10-risk eyes with early or intermediate AMD have thinner retinas as compared to eyes from the Ch

153 f 1 eye of consecutive early or intermediate AMD patients at the Doheny UCLA Eye Centers.

154 d the sMS in eyes with early or intermediate AMD.

155 8 eyes of 488 participants with intermediate AMD at baseline.

156 Six eyes of 4 patients with intermediate AMD each were imaged 4 times over 3.5 years.

157 hy controls and 5 patients with intermediate AMD, before and after photopigment bleaching, were used

158 y of rare variants was compared between late AMD patients and control individuals with logistic regre

159 nts with the largest difference between late AMD patients and control participants and the highest PA

160 nent interacted with CFH rs10922109 for late AMD (P = 0.01 and P = 0.0005, respectively); higher aMed

161 For fish consumption, HRs for late AMD in quartile 4 versus 1 were 0.69 (0.58-0.82, P < 0.0

162 l study visits and graded centrally for late AMD.

163 l study visits and graded centrally for late AMD.

164 6.56; P = 0.0003) genes was observed in late AMD patients compared with control individuals.

165 25.1% in intermediate AMD, and 51.1% in late AMD.

166 at intermediate to high genetic risk of late AMD and enables differential diagnosis of AMD-mimicking

167 vorable lifestyle increased the risk of late AMD at least 2-fold.

168 ly (P <= 0.0005) with decreased risk of late AMD: vitamin A, vitamin B6, vitamin C, folate, beta-caro

169 ny AMD, early AMD, intermediate AMD, or late AMD, geographic atrophy, and neovascular AMD were 18.2%

170 The AUC for predicting late AMD development was similar for the models based on CFP

171 Of the late AMD patients, 1581 of 1777 (89%) showed a positive total

172 minent genetic pathways contributing to late AMD (positive GRS, 90% of patients with late disease), b

173 ociation between PRO scores and time to late AMD in either eye.

174 Genetic risk variants contribute to late AMD in most patients.

175 ur predictive models for progression to late AMD or atrophic AMD were only developed (each including

176 for reducing the risk of progression to late AMD, these 2 studies also confirmed the importance of hi

177 d with decreased risk of progression to late AMD.

178 h intervals to determine progression to late AMD.

179 of the 13 204 eyes, 34.0% progressed to late AMD.

180 observed a higher GRS for patients with late AMD compared with patients with early/intermediate AMD (

181 ate biological interactions between the main AMD disease pathways and suggests that multiple pathways

182 Metabolome-AMD associations were studied using univariate logistic

183 clinically be limited to the eye, mimicking AMD.

184 Here we show in a neovascular AMD mouse model that NLRP3 inflammasome activation in no

185 ate AMD, geographic atrophy, and neovascular AMD were 18.2% (95% confidence interval [CI], 16.8-19.6)

186 Eyes that developed neovascular AMD were censored at the day of its detection.

187 r for the formation of exudative neovascular AMD, there is evidence suggesting a protective effect in

188 ons are stronger for GA than for neovascular AMD.

189 el range of baseline features in neovascular AMD.

190 to guide treatment decisions in neovascular AMD.

191 Exclusion criteria included neovascular AMD in the intervention eye, glaucoma with intraocular p

192 ence of subclinical nonexudative neovascular AMD in the fellow eyes of patients with unilateral exuda

193 stence of a nonexudative form of neovascular AMD would suggest that the term "neovascular AMD" should

194 mprove therapeutic management of neovascular AMD, avoid discrepancies between clinicians/investigator

195 the laser-induced mouse model of neovascular AMD.

196 Regarding neovascular AMD, 9 nutrients were associated nominally with decrease

197 AMD would suggest that the term "neovascular AMD" should be preceded by either "exudative" or "nonexu

198 e signal was greater for GA than neovascular AMD.

199 ions could affect progression to neovascular AMD (nAMD).

200 isease activity in patients with neovascular AMD.

201 ivity while monitoring eyes with neovascular AMD.

202 raphy, RPD were seen in 2.4% of eyes with no AMD or aging changes, 11.5% in early AMD, 25.1% in inter

203 AMD- and non-AMD participants had a similar prevalence and new onset

204 Prevalence of depression in AMD and non-AMD participants was 7.2% and 8.0%, respectively and pre

205 kine profile that was similar to that of non-AMD individuals.

206 Nonexudative AMD severity and presence of central GA also impacted re

207 tive AMD (1.5%), drusen (0.8%), nonexudative AMD (0.3%), toxic maculopathy (0.1%), and hereditary dys

208 ith exudative AMD compared with nonexudative AMD but is unaffected by anti-VEGF treatments, suggestin

209 This Early Biomarkers of AMD (EBAMD) study evaluates serum factors that protect f

210 structural and functional characteristics of AMD.

211 Using clinical classification of AMD with color photography, RPD were seen in 2.4% of eye

212 masked grading in an "evaluation" cohort of AMD eyes with large drusen to determine the predictive v

213 anding of early RPE changes in the course of AMD, potentially before clinical signs appear.

214 ed genes (CFHR1-5) are major determinants of AMD susceptibility, but their molecular consequences rem

215 te AMD and enables differential diagnosis of AMD-mimicking dystrophies.

216 We investigated the genetic distribution of AMD-associated risk variants in a large European consort

217 e detected in eyes without other features of AMD and could represent an earlier disease state.

218 A hallmark of AMD is the overproduction of lipid- and protein-rich ext

219 seen in the absence of drusen, a hallmark of AMD.

220 complement activation levels, independent of AMD status.

221 complement activation levels, independent of AMD status.

222 Significantly, in a mouse model of AMD, this 5A peptide altered the proteomic profile of ci

223 vascular contribution to the pathogenesis of AMD.

224 es in imaging have expanded the phenotype of AMD to include another extracellular deposit, reticular

225 sed to estimate the predicted probability of AMD at 36 months.

226 editerranean diet in reducing progression of AMD in persons with varying severity of disease.

227 e activity is involved in the progression of AMD.

228 , potentially, prevention and remediation of AMD.

229 e assessment of disease severity and risk of AMD progression.

230 igh predictive value of baseline severity of AMD for disease progression.

231 eyes with no clinically observable signs of AMD, the deletion of CFHR1/3, which is strongly protecti

232 the onset of clinically observable signs of AMD.

233 e" when describing this neovascular stage of AMD.

234 uments to record PROs in the early stages of AMD have the potential to produce inexpensive and effici

235 intervention trials for the early stages of AMD to improve their feasibility substantially.

236 In Asian patients, treatment of AMD with anti-VEGF therapy yielded 12-month visual outco

237 d simultaneously for successful treatment of AMD.

238 An online AMD histopathologic resource was reviewed.

239 ch reactor data and used to identify optimum AMD-HFFF mixing ratios that maximize total removal effic

240 er, higher 52-single nucleotide polymorphism AMD genetic risk score was not associated with increased

241 The Ranibizumab AMD Clinical Efficacy in Real-world practice (RACER) stu

242 reports a genotype assay for common and rare AMD genetic variants, which can identify individuals at

243 hin as well as fish consumption are reported AMD risk factors.

244 sted as likely causative genes at respective AMD susceptibility loci.

245 s with BrM represents a new strategy to slow AMD progression in humans.

246 In some AMD patients, marked alterations in the pattern of AO-IR

247 ally, the protective allele of the strongest AMD-associated CFH locus variant rs10922109 has the high

248 Qualitative structural AMD features and SD-OCT-based quantitative thickness cha

249 age patients with AMD, researchers who study AMD disease interventions and pathogenesis, and those wh

250 ural end points in clinical trials targeting AMD stages earlier than atrophy expansion.

251 The AMD prevalence was lower than in Europeans and higher th

252 types was not significantly different in the AMD patients compared to that of controls (P = 0.18).

253 ssociations between the vast majority of the AMD-associated metabolites and systemic complement activ

254 value = 2.2 x 10(-56)), independently of the AMD-protective CFHR1-3 deletion, and even in those indiv

255 in-altering variants in 13 genes outside the AMD-GWAS loci in three or more families.

256 s that underlie the transition from aging to AMD, one of which is a newly developed Center-Surround m

257 real anti-VEGF therapy for type 1 MNV due to AMD.

258 cal effects, as dysfunction of RPEs leads to AMD.

259 ts with geographic atrophy (GA) secondary to AMD (GATHER1 Study).

260 fore the development of atrophy secondary to AMD.

261 association study included 216 advanced type AMD patients and 191 healthy individuals for evaluation.

262 nd wet age-related macular degeneration (wet AMD) have been found to have elevated levels of Tumor Ne

263 or wet age-related macular degeneration (wet AMD), Luxturna for retinitis pigmentosa, Dextenza (0.4 m

264 hanistic role of CD163(+) macrophages in wet AMD pathologies of angiogenesis and leakage of blood com

265 Investigation of Efficacy and Safety in Wet AMD) trial.

266 D163) was elevated only in patients with wet AMD (P < .05).

267 in the peripheral blood of patients with wet AMD, patients with dry AMD, and in age-matched individua

268 led that anti-VEGF treated patients with wet AMD, who showed no exudative signs on the day of blood d

269 as only sometimes seen in normal eyes, while AMD patients exhibited highly variable patterns of alter

270 Counseling individuals affected with AMD regarding the use of the AREDS2 supplements and the

271 Lipoprotein levels were associated with AMD-associated genetic variants, whereas decreased essen

272 degeneration (AMD) and its association with AMD in a large European cohort with relatively good visu

273 owever, despite the genetic association with AMD progression, prediction models found genetic informa

274 A total of 98 eyes diagnosed with AMD of 59 patients (40 female, 19 male) with a mean (+/-

275 nal multimodal imaging features in eyes with AMD associated with GA, risk of progression to GA, or bo

276 nificant reduction of GA growth in eyes with AMD over a 12-month period.

277 longitudinal multimodal imaging of eyes with AMD.

278 individuals from 63 multiplex families with AMD and analyzed the data for rare protein-altering vari

279 ior to optimizing the treatment of HFFF with AMD.

280 ranged from -3.50 to 4.63 and increased with AMD severity.

281 objectives were to assess interactions with AMD genotype.

282 Patients with AMD and PCV received 5.5 and 5.3 injections (5.0 monothe

283 Patients with AMD gained 4.7 logMAR letters after 12 months (P = 0.002

284 Patients with AMD were enrolled in a prospective swept-source optical

285 Patients with AMD who underwent tube revision for erosion at the Duke

286 nhibition of HtrA1 activity in patients with AMD who were treated with the HtrA1-blocking Fab fragmen

287 seful to clinicians who manage patients with AMD, researchers who study AMD disease interventions and

288 rent glaucoma tube erosions in patients with AMD.

289 arch and medical management of patients with AMD.

290 E layer in healthy retinas and patients with AMD.

291 People with AMD often find it difficult to access, process and under

292 rity of online PEMs designed for people with AMD were written above the recommended readability level

293 education materials designed for people with AMD.

294 ess) of online PEMs designed for people with AMD.

295 ure in Caucasian offspring of parent(s) with AMD.

296 ites that were associated significantly with AMD, including increased levels of large and extra-large

297 visual pigment synthesis rates in those with AMD (v = 0.043 SD 0.019 min(-1) and v = 0.119 SD 0.046 m

298 t differences between those with and without AMD.

299 iate AMD (P < 0.001) and individuals without AMD (P < 0.001).

300 AMD, and in age-matched individuals without AMD as controls.