Age-related macular degeneration (AMD) is a complex multifactorial disease characterized in its late form by neovascularization (wet type) or geographic atrophy of the retinal pigment epithelium cell layer (dry type). The complement system is an intrinsic component of innate immunity. There has been growing evidence that the complement system plays an integral role in maintaining immune surveillance and homeostasis in AMD. Based on the association between the genotypes of complement variants and AMD occurrence and the presence of complement in drusen from AMD patients, the complement system has become a therapeutic target for AMD. However, the mechanism of complement disease propagation in AMD has not been fully understood. This concise review focuses on an overall understanding of the role of the complement system in AMD and its ongoing clinical trials. It provides further insights into a strategy for the treatment of AMD targeting the complement system.

Although morphological changes in microglia have been reported to be associated with diabetic retinopathy, little is known about the early changes in the microglia and macrophages during the progression of this condition. The present study was aimed at characterizing retinal microglial activation in the early stages of experimental diabetic retinopathy. Toward this end, a model of diabetic retinopathy was generated by intraperitoneally injecting male Sprague-Dawley rats with streptozotocin. No apparent histological changes were observed during the early stages of experimental diabetic retinopathy. However, at 4 to 16 weeks after the onset of diabetes, the retinas from diabetic rats exhibited higher density of microglia than those from age-matched normal controls, with microglial density peaking at 12 weeks. In particular, the proportion of the activated microglia increased significantly in the diabetic rats, specifically in the nerve fiber and ganglion cell layers, whereas it decreased in the inner plexiform layer within 12 weeks. Furthermore, the resident retinal microglial cells were activated immediately after diabetes induction, peaked at 12 weeks, and remained for up to 16 weeks after disease onset. Thus, experimental diabetic retinopathy causes gradual hypoxia and neuroinflammation, followed by the activation of microglia and the migration of macrophages. The distribution and density of retinal microglial activation changed typically with the progression of the disease in early-stage diabetic rats.

The aim of this study was to investigate foveal and parafoveal microvascular changes in retinal vascular plexuses in patients with type 2 diabetes mellitus (DM) without clinical diabetic retinopathy (NDR) using optical coherence tomography angiography (OCTA) in South Korea. We included 64 patients in the NDR group and included 48 healthy control subjects for comparison. All subjects underwent ocular examination with visual acuity and wide-field fundus photos. Foveal and parafoveal vessel density and foveal avascular zone (FAZ) area (mm²) in the superficial capillary plexus (SCP) and deep capillary plexus (DCP) were analyzed. Foveal vessel densities in both the SCP and DCP were decreased in the NDR group compared to the controls (p=0.034 and 0.001, respectively). Vessel densities in the superior and inferior parafoveae in the DCP were decreased in the NDR group compared to the controls (p=0.006 and 0.034, respectively). The FAZs of the SCP and DCP were significantly different between the NDR group and the controls (p=0.003 and 0.001, respectively). The average vessel densities of the SCP and DCP were not correlated with HbA1c, serum creatinine, or the duration of DM in the NDR group. We demonstrated that OCTA can identify early-stage DR before the manifestation of clinically apparent retinopathy in diabetic eyes. Diabetic patients without clinical DR have microvascular alterations (foveal vessel density, parts of the parafovea, and enlarged FAZ) in the SCP and DCP. Our results suggest that OCTA might be a promising tool for early detection of eyes with DR.

Retinal angiomatous proliferation (RAP) has been known as a variant of exudative age-related macular degeneration (AMD) with a unfavorable prognosis. To evaluate the effect of ranibizumab administered initially as three loading doses for patients with various stages of RAP. A retrospective chart review of 40 patients (41 eyes) with RAP was conducted. The study divided patients into three groups of Group I (8 eyes in stage I), Group II (17eyes in stage II), and Group III (16 eyes in stage III). All patients received three initial monthly intravitreal injections (0.5 mg) of ranibizumab and were monitored monthly for 12 months. Reinjection of ranibizumab after three initial monthly doses was administered on as-needed basis. The main outcome measures were the change in the mean of best-corrected Snellen visual acuity (BCVA) and central macular thickness (CMT), and the total number of injections received during the 12 months. The mean change in BCVA at 12 months was-0.286,-0.165, and-0.151 (logMAR) in Group I, II, and III, respectively. CMT was also reduced by a mean of 32.72 ± 56.75, 57.45 ± 56.48 and 148.37 ± 98.59 μm. The mean number of injections in Group I was significant lower than those in Group II and III (P < 0.001, P < 0.001, and P = 0.15 for Group I versus Group II, Group I versus Group III, and Group II versus Group III, respectively). The 12-month follow-up outcomes suggest that three consecutive loading doses of intravitreal ranibizumab is an effective treatment on early stage (stage I) of RAP. Patients in stage I showed a significantly lower recurrence rate than patients in later stages.

Purpose: We aimed to evaluate microvascular changes on optical coherence tomography angiography (OCTA) in patients with rhegmatogenous retinal detachment (RRD) who underwent silicone oil (SO) tamponade and compare changes according to macular involvement. Methods: This retrospective study included 48 patients with unilateral RRD who underwent vitrectomy and SO tamponade and were stable after SO removal. Control data were obtained from the fellow healthy eye. Ophthalmic examinations, including best corrective visual acuity (BCVA) and OCTA, were conducted. Differences in vascular density (VD) in different sections of the macula and differences in the foveal avascular zone (FAZ) were analyzed between the affected eyes and control eyes. Subgroup analyses according to macular involvement were performed. Results: Baseline BCVA and duration of SO tamponade were associated with postoperative BCVA (p<0.001, p = 0.03, respectively). The average VD in the deep capillary plexus (DCP) and the VD of the nasal parafoveal area in both the superficial capillary plexus (SCP) and the DCP decreased relative to those in the control eyes (p = 0.026, p = 0.028, and p = 0.031, respectively). The FAZ area in the DCP and in the SCP also increased when compared with that in the controls (p = 0.043, p = 0.002, respectively). In addition, the macular-off RRD group had lower VD in the nasal parafoveal area of the DCP than the macular-on RRD group. Conclusion: SO tamponade could cause microvascular changes, especially in the nasal parafoveal area. The macular-off RRD group were affected more than the macular-on RRD group.

Purpose. We aimed to describe the visual prognosis of eyes with ectopic inner foveal layers (EIFLs) after epiretinal membrane (ERM) surgery. Methods. This retrospective study enrolled patients diagnosed with stage 3 ERM based on the EIFL staging scheme who underwent ERM surgery with a minimum follow-up period of 12 months. Central foveal thickness (CFT), EIFL thickness, and the length of the ellipsoid zone defect were evaluated at baseline and at 1 month, 6 months, and 12 months after surgery based on pre- and postoperative swept-source optical coherence tomography (OCT) images. The association of EIFL thickness and other OCT parameters with pre- and postoperative best-corrected visual acuity (BCVA) was analyzed. Results. Sixty-nine eyes with stage 3 ERMs were analyzed. Preoperative BCVA was correlated with preoperative CFT (r = 0.517, ) and preoperative EIFL thickness (r = 0.652, ). At 12 months, postoperative BCVA was correlated negatively with preoperative CFT (r = 0.470, ) and preoperative EIFL thickness (r = 0.582, ). The improvement in BCVA was not associated with postoperative reduction in CFT , although it was significantly associated with postoperative reduction in EIFL thickness (r = 0.635, ). Conclusions. EIFL thickness should be considered a negative prognostic factor for postoperative anatomical and functional recovery in patients with stage 3 ERMs.