ABSTRACT
@#Retina and optic nerve both originate in brain, therefore they have the similar structure and functional characteristics of the brain. Exploring the performance of the central optic nervous disorder on the retina will be beneficial to uncovering the interaction mechanism between brain and eye. As an extension of the central nervous system, the retina contains ganglion cell, a special neuron, whose axon form the optic nerve and has access into the central nervous system. Therefore, the retina can be used as a mirror reflecting neurodegenerative diseases structurally and functionally. With the development of imaging technology, optical coherence tomography(angiography)has become the mainstream tool for ophthalmological clinical diagnosis due to its easy operation and low cost. In recent years, discovering biomarkers of neurodegenerative diseases, especially Alzheimer's disease, Parkinson's disease, multiple sclerosis and so on, in the retinal optical coherence tomography images has gradually become an emerging research direction. In this review, we summarized the research progress of neurodegenerative diseases analysis based on the retinal images in the past decade, and provide a prospect to inspire further research as far as possible.
ABSTRACT
@#AIM: To evaluate the differences of macular vascular network measured by optical coherence tomography angiography(OCTA)between severe non-proliferative diabetic retinopathy(S-NPDR)eyes and health eyes, and explore the changes of these OCTA characteristics in patients with S-NPDR before and after panretinal photocoagulation(PRP).<p>METHODS: This was a prospective study including 31 eyes from 18 consecutive patients with S-NPDR and 31 eyes of healthy subjects. We measured macular vascular density and foveal avascular zone(FAZ)area and volume by an OCTA device.<p>RESULTS: Compared to the normal control group, in superficial retinal capillary plexus(SCP), macular vascular density decreased in S-NPDR group, except foveal vascular density unchanged. Consistently, in deep retinal capillary plexus(DCP), macular vascular density was also lower in S-NPDR group. In addition, FAZ area and volume expanded in S-NPDR eyes. At 6mo post-PRP in S-NPDR eyes, foveal SCP and DCP densities increased significantly, while FAZ area and volume decreased. At 3mo post-PRP, only foveal vascular density in DCP increased. The changes of foveal SCP and DCP densities as well as FAZ area and volume were not statically significant at 1mo post-PRP.<p>CONCLUSION: Macular vascular network was impaired in S-NPDR assessed by OCTA. Although OCTA parameters were not significantly affected by PRP in 1 and 3mo period, at 6mo follow-up parameters became significant after PRP.
ABSTRACT
Diabetic retinopathy (DR), one of the most serious complications of diabetes, has been associated with inflammatory processes. We have recently reported that interleukin (IL)-17A, a proinflammatory cytokine, is increased in the plasma of diabetic patients. Further investigation is required to clarify the role of IL-17A in DR. Ins2(Akita) (Akita) diabetic mice and high-glucose (HG)-treated primary Müller cells were used to mimic DR-like pathology. Diabetes induced retinal expression of IL-17A and IL-17 receptor A (IL-17RA) in Müller cells in contrast to ganglion cells. Further evidence demonstrated that retinal Müller cells cultured in vitro increased IL-17A and IL-17RA expression as well as IL-17A secretion in the HG condition. In both the HG-treated Müller cells and Akita mouse retina, the Act1/TRAF6/IKK/NF-κB signaling pathway was activated. IL-17A further enhanced inflammatory signaling activation, whereas Act1 knockdown or IKK inhibition blocked the downstream signaling activation by IL-17A. HG- and diabetes-induced Müller cell activation and dysfunction, as determined by increased glial fibrillary acidic protein, vascular endothelial growth factor and glutamate levels and decreased glutamine synthetase and excitatory amino acid transporter-1 expression, were exacerbated by IL-17A; however, they were alleviated by Act1 knockdown or IKK inhibition. In addition, IL-17A intravitreal injection aggravated diabetes-induced retinal vascular leukostasis, vascular leakage and ganglion cell apoptosis, whereas Act1 silencing or anti-IL-17A monoclonal antibody ameliorated the retinal vascular damage and neuronal cell apoptosis. These findings establish that IL-17A exacerbates DR-like pathology by the promotion of Müller cell functional impairment via Act1 signaling.