EXPLORING BECLIN-1 THERAPEUTIC POTENTIAL IN NEURODEGENERATIVE DISEASES: FOCUS ON MULTIPLE SCLEROSIS

In MS (Multiple Sclerosis) and other neurological illnesses, autophagy protein Beclin-1 is crucial. Self-eating, a critical neuroprotective function, is faulty; neurodegenerative illnesses have low Beclin-1 expression; hazardous protein clusters are not eliminated. This study investigates if Beclin-1 may target cell metabolism in an experimental MS model. This cross-sectional study examined Beclin-1, oxidative stress biomarkers, and pro-inflammatory cytokines in 100 MS patients and 100 age- and sex-matched healthy controls. Quantifying Beclin-1's signaling pathway interactions required molecular docking. The study also examined how Beclin-1 overexpression affected disease onset, inflammation, and demyelination in MS patients (n=30). The study used an ANOVA test to evaluate data, with a significance threshold of p<0.05. In this study, MS patients had lower serum Beclin-1 concentrations (3.15±0.45 ng/ml) compared to the control group (5.02±0.60 ng/ml). Increased MDA (7.33±1.12 µM vs. 4.21±0.90 µM in the control group) and TNF-α levels (21.25±2.30pg/ml vs. 10.12±1.70 pg/ml in the control group). The MS patients with Beclin-1 overexpression demonstrated improved motor function, 25% less demyelination, and 15% less production of pro-inflammatory cytokines including IL-6 and IL-1β. Several computer studies demonstrated that Beclin-1 may bind to other autophagic pathway proteins and be effective in treatment. Beclin-1 shortage is a crucial component in MS and its restoration can minimize neuronal damage owing to defective autophagy and excessive inflammation. These facts indicate the need for a fresh understanding of Beclin-1-focused therapy in MS.