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The response discusses ganglion cell layer and inner plexiform layer thinning as a possible sign of early neurodegenerative change, links early diabetic retinopathy to disrupted glutamate metabolism and Müller cell/ganglion cell apoptosis, and highlights corneal nerve alterations. It also notes associations between male sex, higher BMI, longer axial length and thicker central retina, and proposes further investigation of topical neuroprotective drugs to delay progression and reduce need for invasive 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and contrast sensitivity in early diabetic retinopathy  \nDear Editor,  \nIn the response to the article titled “Optical coherence tomography and contrast sensitivity in early diabetic retinopathy”published in your esteemed journal, which is a well‑thought‑out and written paper, I would like to raise few points regarding this study.  \nThe article concluded that the reduced thickness of the ganglion cell layer + inner plexiform layer is possibly indicative of early neurodegenerative changes in the inner retina.[1]  \nThe early alterations in diabetic retinopathy are caused by disruptions in glutamate metabolism, which has been shown to have reduced oxidation in theretinasof diabetic rats (62%, P \u003C 0.05) . Additionally, there is a reduction in the activity of glutamine synthetase (ranging from 48%[P \u003C 0.005] to 83%[P \u003C 0.05] compared to controls) . This leads to an accumulation of glutamate, which triggers apoptosis in Müller cells and retinal ganglion cells, contributing to neurodegeneration.[2]  \nNeurodegenerative changes in diabetes can also affect the cornea. A study evaluating 132 eyes of patients with type 2 diabetes using confocal microscopy observed a reduction in nerve fiber density, branching, and length in the corneal nerve layer of diabetic patients. The study’s findings support the theory that nerve fiber damage precedes the development of diabetic retinopathy, indicating a neurodegenerative process independent of microvascular changes.[3]  \nIt is important to consider in the evaluation of diabetic patients that male individuals, with a higher body mass index and longer axial length, are associated with a thicker central retina.[4]  \nThese studies suggest that the topical application of neuroprotective medications may be useful in  \npreventing the worsening of neurodysfunction in diabetic retinopathy. Therefore, the use of topical neuroprotective drugs (brimonidine and somatostatin) should be further investigated in this patient group, potentially preventing the need for more invasive treatments such as intravitreal antivascular endothelial growth factor injections and laser therapy.[5]  \nData availability statement  \nData sharing isnot applicable to this article as no datasets were generated or analyzed during the current study.  \nFinancial support and sponsorship  \nNil.  \nConflicts of interest  \nAll authors have completed and submitted the ICMJE Form for disclosure of potential conflicts of interest and none were reported.  \nThiago Gonçalves Dos Santos Martins1*, Diogo Gonçalves Dos Santos Martins2  \n1Federal University of Rio de Janeiro, Rio de Janeiro, 2Federal University of São Paulo, São Paulo, Brazil  \n*Address for correspondence:  \nDr. Thiago Gonçalves Dos Santos Martins, Botucatu Street, 821 Vila Clementino, São Paulo, Brazil.  \nE-mail: [thiagogsmartins@yahoo.com.br](thiagogsmartins@yahoo.com.br)  \nSubmission: 13-09-2024  \nAccepted: 03-11-2024  \nPublished: 26-03-2025  \nReferences  \n1. Ostadimoghadam H, Helmi T, Yekta A, Shandiz JH, Shafaei H, Moghadam HM, et al. Optical coherence tomography and contrast sensitivity in early diabetic retinopathy. Taiwan J Ophthalmol 2024;14:403‑8 .  \n2. Lieth E, LaNoue KF, Antonetti DA, Ratz M. Diabetes reduces glutamate oxidation and glutamine synthesis in the  \n668 © 2025 Taiwan J Ophthalmol | Published by Wolters Kluwer-Medknow  \nretina. The Penn State Retina Research Group. Exp Eye Res 2000;70:723‑30 .  \n3. Bitirgen G, Ozkagnici A, Malik RA, Kerimoglu H. Corneal nerve fibre damage precedes diabetic retinopathyin patients with type 2 diabetes mellitus. Diabet Med 2014;31:431‑8 .  \n4. Wong AC, Chan CW, Hui SP. Relationship of gender, body mass index, and axial length with central retinal thickness using optical coherence tomography. Eye (Lond) 2005;19:292‑7 .  \n5. Simó R, Hernández C, Porta M, Bandello F, Grauslund J, Harding SP, et al. Effects of topically administered neurop","cbCaimGUfDD11eIK","https://ap.wps.com/l/cbCaimGUfDD11eIK","pdf",236247,"English","# Letter to the Editor\n## Key clinical and mechanistic points\n## Data availability and disclosures","[{\"question\":\"What neurodegenerative mechanism does the letter connect to early diabetic retinopathy?\",\"answer\":\"It links early alterations to disrupted glutamate metabolism, leading to glutamate accumulation that triggers apoptosis in Müller cells and retinal ganglion cells, contributing to neurodegeneration.\"},{\"question\":\"How does the letter describe evidence from the cornea in diabetes?\",\"answer\":\"A cited confocal microscopy study in patients with type 2 diabetes found reduced corneal nerve fiber density, branching, and length, supporting the idea that nerve damage can precede diabetic retinopathy.\"},{\"question\":\"Which treatments does the letter propose for further investigation, and why?\",\"answer\":\"It suggests evaluating topical neuroprotective medications such as brimonidine and somatostatin, aiming to prevent worsening neurodysfunction and potentially avoid more invasive intravitreal injections and laser therapy.\"}]","Comment on optical coherence tomography and contrast sensitivity in early diabetic retinopathy - Letter to the Editor | PDF",1790746435]