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Toxic Advanced Glycation End-Products Inhibit Axonal Elongation Mediated by β-Tubulin Aggregation in Mice Optic
Hayahide Ooi1, Ayako Furukawa1, Masayoshi Takeuchi2
1Graduate School and Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, 3500-3 Minamitamagaki, Suzuka 513-8670, Japan.
Abstract:
Advanced glycation end-products (AGEs) form through non-enzymatic glycation of various proteins. Optic nerve degeneration is a frequent complication of diabetes, and retinal AGE accumulation is strongly linked to the development of diabetic retinopathy. Type 2 diabetes mellitus is a major risk factor for Alzheimer's disease (AD), with patients often exhibiting optic axon degeneration in the nerve fiber layer. Notably, a gap exists in our understanding of how AGEs contribute to neuronal degeneration in the optic nerve within the context of both diabetes and AD. Our previous work demonstrated that glyceraldehyde (GA)-derived toxic advanced glycation end-products (TAGE) disrupt neurite outgrowth through TAGE-β-tubulin aggregation and tau phosphorylation in neural cultures. In this study, we further illustrated GA-induced suppression of optic nerve axonal elongation via abnormal β-tubulin aggregation in mouse retinas. Elucidating this optic nerve degeneration mechanism holds promise for bridging the knowledge gap regarding vision loss associated with diabetes mellitus and AD.
Insights
Advanced glycation end-products (AGEs) cause optic nerve degeneration in diabetes and Alzheimer's disease (AD). This study shows glyceraldehyde-derived AGEs disrupt axonal growth by affecting beta-tubulin in mouse retinas.
Area of Science:
- Neuroscience
- Biochemistry
- Ophthalmology
Background:
- Advanced glycation end-products (AGEs) accumulate in diabetes and are linked to diabetic retinopathy.
- Type 2 diabetes mellitus and Alzheimer's disease (AD) share optic nerve degeneration as a complication.
- The role of AGEs in optic nerve degeneration in diabetes and AD remains unclear.
Purpose of the Study:
- To investigate the mechanism by which AGEs contribute to optic nerve degeneration.
- To elucidate the role of glyceraldehyde (GA)-derived AGEs in axonal growth suppression.
- To explore the link between AGEs, beta-tubulin aggregation, and tau phosphorylation in neuronal degeneration.
Main Methods:
- Utilized mouse retinal explants to study axonal elongation.
- Investigated the effects of GA-derived toxic AGEs (TAGE) on optic nerve axons.
- Examined beta-tubulin aggregation and tau phosphorylation in neural cultures and retinas.
Main Results:
- GA-induced TAGE suppressed optic nerve axonal elongation in mouse retinas.
- Abnormal beta-tubulin aggregation was observed in GA-treated optic nerve axons.
- Previous studies showed TAGE disrupts neurite outgrowth via beta-tubulin aggregation and tau phosphorylation.
Conclusions:
- Glyceraldehyde-derived AGEs contribute to optic nerve degeneration by disrupting axonal growth through beta-tubulin aggregation.
- Understanding this mechanism may bridge the knowledge gap in vision loss associated with diabetes and AD.
- This research provides insights into AGE-mediated neurodegeneration in the optic nerve.
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