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Sialic Acid Mimetic Microglial Sialic Acid-Binding Immunoglobulin-like Lectin Agonism: Potential to Restore Retinal
Michael J Tolentino1,2,3, Andrew J Tolentino4, Elizabeth M Tolentino5
1Department of Ophthalmology, University of Central Florida College of Medicine, Orlando, FL 32827, USA.
Abstract:
Age-related macular degeneration (AMD), a leading cause of visual loss and dysfunction worldwide, is a disease initiated by genetic polymorphisms that impair the negative regulation of complement. Proteomic investigation points to altered glycosylation and loss of Siglec-mediated glyco-immune checkpoint parainflammatory and inflammatory homeostasis as the main determinant for the vision impairing complications of macular degeneration. The effect of altered glycosylation on microglial maintained retinal para-inflammatory homeostasis and eventual recruitment and polarization of peripheral blood monocyte-derived macrophages (PBMDMs) into the retina can explain the phenotypic variability seen in this clinically heterogenous disease. Restoring glyco-immune checkpoint control with a sialic acid mimetic agonist targeting microglial/macrophage Siglecs to regain retinal para-inflammatory and inflammatory homeostasis is a promising therapeutic that could halt the progression of and improve visual function in all stages of macular degeneration.
Insights
Age-related macular degeneration (AMD) involves impaired immune regulation due to genetic factors. Restoring immune checkpoints with sialic acid mimetics may halt AMD progression and improve vision.
Area of Science:
- Ophthalmology
- Immunology
- Genetics
Background:
- Age-related macular degeneration (AMD) is a primary cause of global vision loss.
- Genetic factors impairing complement regulation initiate AMD.
- Altered glycosylation and loss of Siglec-mediated immune checkpoints contribute to AMD pathogenesis.
Purpose of the Study:
- To investigate the role of altered glycosylation and Siglec-mediated checkpoints in AMD.
- To explore the impact of these changes on microglial homeostasis and macrophage recruitment.
- To evaluate a novel therapeutic strategy for AMD.
Main Methods:
- Proteomic analysis to identify key molecular changes.
- Investigated the effect of altered glycosylation on microglial and macrophage function.
- Assessed the potential of sialic acid mimetics as a therapeutic intervention.
Main Results:
- Altered glycosylation and Siglec pathway disruption are central to AMD complications.
- These changes affect retinal para-inflammatory homeostasis and monocyte-derived macrophage polarization.
- The findings explain the clinical heterogeneity observed in AMD patients.
Conclusions:
- Restoring glyco-immune checkpoint control is a promising therapeutic avenue for AMD.
- Sialic acid mimetics targeting microglial/macrophage Siglecs can restore homeostasis.
- This approach holds potential to halt AMD progression and enhance visual function across all disease stages.
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