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Emerging Insights into Pathogenesis.

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    Diabetic retinopathy (DR) involves inflammation and neurodegeneration, not just vascular issues. Early signs in diabetes include retinal glia cell activation and neural cell loss, even before clinical DR symptoms appear.

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    Area of Science:

    • Ophthalmology
    • Endocrinology
    • Neuroscience

    Background:

    • Diabetic retinopathy (DR) is a common complication of diabetes mellitus (DM).
    • Persistent hyperglycemia triggers inflammation, oxidative stress, and vascular dysfunction in the retina.
    • Emerging evidence indicates inflammation and neurodegeneration precede clinical DR signs.

    Purpose of the Study:

    • Investigate the early inflammatory and neurodegenerative pathways in diabetic retinopathy (DR).
    • Understand the in vivo mechanisms of DR pathogenesis and complications like diabetic macular edema.
    • Explore potential biomarkers and therapeutic targets for DR.

    Main Methods:

    • Analysis of inflammatory mediators, growth factors, and molecules in human aqueous and vitreous humor.
    • Utilizing non-invasive techniques like optical coherence tomography (OCT).
    • Observing in vivo markers such as hyperreflective intraretinal spots.

    Main Results:

    • Retinal glia cells (RGC), including microglia and macroglia, are activated early in diabetes.
    • Activated RGC contribute to inflammation, blood-retinal barrier breakdown, and neuronal cell death.
    • OCT detects hyperreflective spots and early neural cell loss, indicating in vivo microglial activation and neurodegeneration.

    Conclusions:

    • DR pathogenesis involves both inflammation and neurodegeneration, starting before clinical manifestation.
    • Early RGC activation and neural cell loss are key features of diabetes-related retinopathy.
    • Understanding these early events offers new avenues for DR diagnosis and treatment.