ArticleJournal of molecular neuroscience : MN2025
The Astrocyte Elevated Gene- 1 Expression and other Risk Factors for Different Varieties of Diabetic Optic Neuropathy in Egyptian Patients with Diabetic Retinopathy.
Article in Journal of molecular neuroscience : MN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
To assess the role of the mRNA and protein expression of Astrocyte Elevated Gene- 1 (AEG-1) and other possible risk factors for diabetic optic neuropathy (DON) in Egyptian patients with diabetic retinopathy (DR). This case-control study constituted 450 diabetic patients divided into three groups: Group 1 included 150 DR patients with any sign of DON (diabetic papillopathy (DP), non-arteritic anterior ischemic optic neuropathy (AION), and optic atrophy (OA)). Group 2 included 150 DR patients without any sign of DON. Group 3 included 150 sex and age-matched diabetic patients without any sign of DR or DON. The expression level of AEG-1 mRNA was assessed by real-time PCR. Serum AEG-1 was determined by ELISA. Multivariate logistic regression analysis was conducted to assess the DON risk factors. The mRNA expression of the AEG-1 gene and AEG-1 protein levels were significantly increased (P < 0.001) in diabetic patients with (group 1) than without (group 2) DON. ROC curve analysis showed that the mRNA level of the AEG-1 gene exhibited a 70% specificity and a 79.33% diagnostic sensitivity. The diagnostic sensitivity of the serum concentration of AEG-1 was 84.67%, while the specificity was 70%. Multivariate regression analysis showed that the risk factors for DON were 2hpp blood sugar, HbA1c, serum cholesterol, AEG-1 gene's mRNA expression, and AEG-1 protein. Serum cholesterol, the AEG-1 gene's mRNA expression, and the AEG-1 protein are risk factors for all varieties of DON. While the blood glucose levels favour the development of DP, control of diabetes favours the occurrence of AION. Lastly, diabetes duration is more related to the presence of OA.
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