Diabetes mellitus (DM) is a global disease that is strongly associated with both microvascular and macrovascular complications. A significant proportion of individuals with diabetes develop diabetic retinopathy (DR), a microvascular complication that can lead to blindness, particularly in working-age adults. Diabetes adversely affects the entire neurosensory retina, with accelerated neuronal apoptosis and activation or altered metabolism of neuroretinal supporting cells. These findings suggest that DR could be a sensory neuropathy that affects the retinal parenchyma, similar to peripheral diabetic neuropathy. Neurotrophins have been implicated in the progression of DR. This study was done to determine the association of serum brain-derived neurotrophic factor (BDNF) levels with DR in type 2 diabetic patients in a tertiary care hospital in North India.

 A hospital-based case-control study was done. The case group included diabetic patients with retinopathy (n=44) and the control group included diabetic patients without retinopathy (n=44). Serum BDNF levels were estimated by enzyme-linked immunosorbent assay (ELISA). Statistical analysis was carried out using GraphPad Prism software (Dotmatics, Boston, USA).

 The mean serum BDNF in the control and case groups was 2753 ± 465 pg/ml and 1598 ± 483 pg/ml, respectively. The difference between the two groups was statistically significant as per the Mann-Whitney U test (U=64, p<0.0001). Logistic regression analysis showed that BDNF is a good predictor for DR after multivariate regression.

 Patients with DR were found to have lower serum BDNF levels compared to those without retinopathy. BDNF may serve as an early predictor for DR. Due to its role in neuronal health and metabolism, increasing BDNF levels could offer a therapeutic approach to managing diabetes-related complications. However, further research is needed to confirm the effectiveness of BDNF in slowing or preventing the progression of DR.

Non-proliferative diabetic retinopathy (NPDR) poses a significant challenge in diabetes management due to its microvascular changes in the retina. Laser photocoagulation, a conventional therapy, aims to mitigate the risk of progressing to proliferative diabetic retinopathy (PDR).

To compare the efficacy and safety of multi-spot vs single-spot scanning panretinal laser photocoagulation in NPDR patients.

Forty-nine NPDR patients (86 eyes) treated between September 2020 and July 2022 were included. They were randomly allocated into single-spot (n = 23, 40 eyes) and multi-spot (n = 26, 46 eyes) groups. Treatment outcomes, including best-corrected visual acuity (BCVA), central macular thickness (CMT), and mean threshold sensitivity, were assessed at predetermined intervals over 12 months. Adverse reactions were also recorded.

Energy levels did not significantly differ between groups (P > 0.05), but the multi-spot group exhibited lower energy density (P < 0.05). BCVA and CMT improvements were noted in the multi-spot group at one-month post-treatment (P < 0.05). Adverse reaction incidence was similar between groups (P > 0.05).

While energy intensity and safety were comparable between modalities, multi-spot scanning demonstrated lower energy density and showed superior short-term improvements in BCVA and CMT for NPDR patients, with reduced laser-induced damage.

To investigate the relationship between serum brain-derived neurotrophic factor (BDNF) and changes in macular perfusion in different stages of diabetic retinopathy (DR) using optical coherence tomography angiography (OCTA).

The study was conducted on 72 eyes of people with type 2 diabetes mellitus (DM). They were divided into five groups based on their DR stage: no DR (nDR), mild and moderate nonproliferative DR, severe nonproliferative DR, active proliferative DR (aPDR), and stable PDR. The presence or absence of diabetic maculopathy was also used to categorize the cases. All patients underwent a complete history, ophthalmological examination, OCTA imaging, and evaluation of BDNF and glycated hemoglobin A1c levels.

The mean blood BDNF levels in the aPDR group were considerably lower than those in the nDR group (P = 0.023). In comparison to eyes without maculopathy, eyes with maculopathy had considerably decreased mean blood BDNF levels (P = 0.0004). Comparing NPDR and PDR groups to nDR as well as NPDR and PDR, a substantial decrease in average and parafoveal vessel density (VD) of the retina and choriocapillaries was seen (P = 0.02). The Foveal Avascular Zone (FAZ) acircularity index and VD were found to be significantly impacted by deteriorating DR (P = 0.001 and 0.017, respectively). It was discovered that there is a positive correlation between BDNF and the FAZ fractal dimension (P = 0.03). In diabetic eyes, there was a statistically favorable correlation between BDNF levels and best corrected visual acuity (P = 0.002). Furthermore, there was a negative relationship between DM duration and BDNF (P = 0.021).

Serum BDNF levels decreased with the progression of DR and in patients with maculopathy. BDNF was found to be related to macular perfusion, particularly in the fovea.

The possible impact of topiramate against diabetic retinopathy (DREN) and its molecular mechanisms in relation to the nod-like receptor family pyrin domain containing 3 (NLRP3) inflammasome has not been studied before. Thus, in the present study, we aimed to utilize a computational approach to investigate the possible protective effect of topiramate on experimental DREN and explore its impact on NLRP3/interlukin-1β signaling and brain-derived neurotrophic factor (BDNF) expression. Male albino mice were distributed to four experimental groups and assigned the following categorizations: (i) saline, (ii) diabetic, (iii) diabetic + topiramate 10 mg/kg and (iv) diabetic + topiramate 30 mg/kg. We observed shrinkage of total retinal thickness and elevation in retinal glutamate, malondialdehyde, NLRP3 and interlukin-1β but decreased glutathione (GSH) levels in the diabetic mice. Additionally, retinal ultra-structures in the diabetic group showed abnormalities and vacuolations in the pigmented epithelium, the photoreceptor segment, the outer nuclear layer, the inner nuclear layer and the ganglion cell layer (GCL). Mice treated with topiramate 10 or 30 mg/kg showed downregulation in retinal malondialdehyde, NLRP3 and interlukin-1β levels; improvements in the retinal pathologies; enhanced immunostaining for BDNF and improved ultra-structures in different retinal layers. Overall, the current results suggest topiramate as a neuroprotective agent for DREN, and future studies are warranted to further elucidate the mechanism of its protective action.

Background: Diabetic retinopathy (DR) is a neurovascular disease, characterized by a deficiency of brain-derived neurotrophic factor (BDNF), a regulator of autophagy. Beta-hydroxybutyrate (BHB), previously reported as a protective agent in DR, has been associated with BDNF promotion. Here, we investigated whether systemic BHB affects the retinal levels of BDNF and local autophagy in diabetic mice with retinopathy; Methods: C57BL/6J mice were administered with intraperitoneal (i.p.) streptozotocin (STZ) (75 mg/kg) injection to develop diabetes. After 2 weeks, they received i.p. injections of BHB (25−50−100 mg/kg) twice a week for 10 weeks. Retinal samples were collected in order to perform immunofluorescence, Western blotting, and ELISA analysis; Results: BHB 50 mg/kg and 100 mg/kg significantly improved retinal BDNF levels (p < 0.01) in diabetic mice. This improvement was negatively associated with autophagosome−lysosome formations (marked by LC3B and ATG14) and to higher levels of connexin 43 (p < 0.01), a marker of cell integrity. Moreover, BHB administration significantly reduced M1 microglial activation and autophagy (p < 0.01); Conclusions: The systemic administration of BHB in mice with DR improves the retinal levels of BDNF, with the consequent reduction of the abnormal microglial autophagy. This leads to retinal cell safety through connexin 43 restoration.

Chronic diabetic retinopathy (DR) is a diabetic complication that causes blindness. Brain-derived neurotrophic factor (BDNF) expression is induced by fluoxetine. We observed the effects of fluoxetine on a streptozotocin (STZ)-induced diabetic rat model in this study.

Rats were divided into three groups: Control, diabetic (65 mg/kg STZ injection), and diabetic with fluoxetine injection (20 mg/kg/week, six times). Western blotting was performed using anti-BDNF and anti-hexaribonucleotide-binding protein-3. Expression of BCL2 apoptosis regulator-like protein 11 (BIM) was analysed using a reverse transcription-polymerase chain reaction.

BDNF levels were significantly higher in the diabetic group treated with fluoxetine than in the untreated diabetic group. BIM expression was higher in the diabetic group than in the control group. BIM gene expression was lower in fluoxetine-treated diabetic group than in the untreated diabetic group.

Fluoxetine had an anti-apoptotic effect with upregulation of BDNF expression in retina of rats with STZ-induced diabetes.