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This study investigated the role of brain-derived neurotrophic factor (BDNF) in patients with degenerative lumbar stenosis, focusing on its expression and correlation with pain intensity. The study examined 96 patients with lumbar stenosis and 85 control participants. BDNF levels in the yellow ligamentum flavum were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and western blot analysis. The results showed significantly higher BDNF expression at both messenger ribonucleic acid (mRNA; fold change = +1.35 ± 0.23; p < 0.05) and protein levels in patients (28.98 ± 6.40 pg/mg) compared to controls (4.56 ± 1.98 pg/mg; p < 0.05). Furthermore, BDNF levels correlated positively with pain intensity reported by patients, with higher expression observed in those experiencing more severe pain. The study also explored the influence of lifestyle factors, such as smoking and alcohol consumption, and related diseases, such as diabetes, on BDNF expression. Smoking, alcohol use, and diabetes were associated with significantly elevated BDNF levels (p < 0.05). These findings suggest that BDNF could serve as a biomarker for pain severity in degenerative lumbar stenosis at the protein level, although this was not consistently observed at the mRNA level; this highlights the potential for BDNF-targeted therapies in managing pain. Future research should involve larger longitudinal studies to validate these findings and explore therapeutic interventions. This study underscores the importance of considering molecular and lifestyle factors in the treatment of degenerative lumbar stenosis, aiming to improve patient outcomes through comprehensive, targeted approaches. [ABSTRACT FROM AUTHOR]

The study investigates molecular changes in the lumbosacral (L/S) spine's yellow ligamentum flavum during degenerative stenosis, focusing on the role of transforming growth factor beta 1–3 (TGF-β-1–3). Sixty patients with degenerative stenosis and sixty control participants underwent molecular analysis using real-time quantitative reverse transcription reaction technique (RTqPCR), enzyme-linked immunosorbent assay (ELISA), Western blot, and immunohistochemical analysis (IHC). At the mRNA level, study samples showed reduced expression of TGF-β-1 and TGF-β-3, while TGF-β-2 increased by only 4%. Conversely, at the protein level, the study group exhibited significantly higher concentrations of TGF-β-1, TGF-β-2, and TGF-β-3 compared to controls. On the other hand, at the protein level, a statistically significant higher concentration of TGF-β-1 was observed (2139.33 pg/mL ± 2593.72 pg/mL vs. 252.45 pg/mL ± 83.89 pg/mL; p < 0.0001), TGF-β-2 (3104.34 pg/mL ± 1192.74 pg/mL vs. 258.86 pg/mL ± 82.98 pg/mL; p < 0.0001), TGF-β-3 (512.75 pg/mL ± 107.36 pg/mL vs. 55.06 pg/mL ± 9.83 pg/mL, p < 0.0001) in yellow ligaments obtained from patients of the study group compared to control samples. The study did not establish a significant correlation between TGF-β-1–3 concentrations and pain severity. The findings suggest that molecular therapy aimed at restoring the normal expression pattern of TGF-β-1–3 could be a promising strategy for treating degenerative stenosis of the L/S spine. The study underscores the potential therapeutic significance of addressing molecular changes at the TGF-β isoforms level for better understanding and managing degenerative spinal conditions. [ABSTRACT FROM AUTHOR]

Introduction: The role of Brain-Derived neurotrophic Factor (BDnF) in intervertebral disc degeneration may contribute to the pathogenesis of lumbosacral stenosis through its influence on neuronal survival and synaptic plasticity within the spinal canal. Aim: The aim of this study was to determine the differences in expression profiles of BDnF in IVD degeneration and L/S stenosis. Material and methods: The study group comprised 113 patients diagnosed with IVDD who qualified for microdiscectomy. The comparison group included 60 patients with L/S stenosis. The expression profiles of BDnF were determined by enzyme-linked immunosorbent assay (ELISA). Results: The concentration of BDnF in the IVD of patients was 17.91pg/mL ±19.58 pg/mL, while in the yellow ligament of patients with L/S spinal degenerative stenosis was 4.97 pg/mL ±0.25 pg/m (p<0.05). Conclusions: In conclusion, our study highlights significant differences in the expression profiles of Brain-Derived neurotrophic Factor (BDnF) between intervertebral disc degeneration (IVDD) and lumbosacral (L/S) spinal degenerative stenosis. We found that the concentration of BDnF in the intervertebral discs of patients with IVDD was notably higher compared to that in the yellow ligament of patients with L/S stenosis. This suggests a potential role of BDnF in the pathogenesis of IVDD, possibly through its influence on neuronal survival and synaptic plasticity within the spinal canal. These findings shed light on the molecular mechanisms underlying spinal degenerative disorders and may pave the way for targeted therapeutic interventions aimed at modulating BDnF expression to mitigate disc degeneration and associated symptoms. Further research is warranted to elucidate the exact mechanisms by which BDnF contributes to these pathologies and to explore its potential as a therapeutic target. [ABSTRACT FROM AUTHOR]

Introduction: Unhealthy habits such as overeating processed and high-calorie foods, alcohol abuse, and smoking negatively impact human health. It has been suggested that the inflammatory process and the resulting growth of nerve fibers within the intervertebral disc (IVD) fissures is the main reason for the pain accompanying IVD degeneration (IVDD). Aim: The aim of this study was to determine whether smoking, alcohol consumption, overweight/obesity, or diabetes comorbidity contribute to the development of IVDD and how the aforementioned factors affect the levels of brain-derived neurotrophic factor (BDnF), glial cell-derived neurotrophic factor (GDnF), and growth associated protein 43 (GAP-43) in the study and control groups. Material and methods: The study group comprised 113 patients diagnosed with IVDD who qualified for microdiscectomy. Control group included 81 IVDs obtained from Caucasian human cadavers. The expression profiles of BDnF, GDnF, and GAP-43 were determined by enzyme-linked immunosorbent assay (ELISA). Results: Our statistical analysis confirmed that patients who were overweight/obese, smoked tobacco, consumed alcohol, or had diabetes had a higher risk of IVDD (OR>1). Statistical analysis showed that BDnF, GAP-43, and GDnF concentrations were significantly higher in the IVDs obtained from the study group compared with the control group (p<0.05). In addition, higher levels of BDnF, GDnF, and GAP-43 were noted in IVDD patients who consumed alcohol, smoked tobacco, were overweight/obese, or had comorbid diabetes compared with patients without these risk factors (p<0.05). Conclusions: We showed that changes in energy metabolism, habits, and lifestyle as well as the degenerative process of IVD in the lumbosacral spine contribute to changing the concentration profile of the analyzed neurotrophic factors. [ABSTRACT FROM AUTHOR]

Introduction: The clinical manifestation of degenerative stenosis of the lumbosacral (L/S) spine also has a molecular basis. Aim: The study investigates molecular changes in the L/S spine's ligamentum flavum during degenerative stenosis, focusing on the role of transforming growth factor beta 1-3 (TGF-α1-3). Material and methods: Sixty patients with degenerative stenosis and sixty control participants underwent molecular analysis using real-time quantitative reverse transcription reaction technique (RTqPCR), enzyme-linked immunosorbent assay (ELISA), Western blot, and immunohistochemical analysis (IHC). Results: At the mRnA level, study samples showed reduced expression of TGF-α1 and TGF-α3, while TGF-α2 increased by only 4%. Conversely, at the protein level, the study group exhibited significantly higher concentrations of TGF-α1, TGF-α2, and TGF-α3 compared to controls. On the other hand, at the protein level, a statistically significant higher concentration of TGF-β1 was observed (2139.33 pg/ml±2593.72 pg/ml vs. 252.45 pg/ml±83.89 pg/ml; p<0.0001), TGF-α2 (3104.34 pg/ml±1192.74 pg/ml vs. 258.86 pg/ml±82.98; p<0.0001), TGF-α3 (512.75 pg/mL±107.36 pg/mL vs. 55.06 pg/mL±9.83 pg/mL, p<0.0001) in yellow ligaments obtained from patients of the study group compared to control samples. The study did not establish a significant correlation between TGF-α1-3 concentrations and pain severity. Conclusions: The findings suggest that molecular therapy aimed at restoring the normal expression pattern of TGF-α1-3 could be a promising strategy for treating degenerative stenosis of the L/S spine. The study underscores the potential therapeutic significance of addressing molecular changes at the TGF-α isoform level for better understanding and managing degenerative spinal conditions. [ABSTRACT FROM AUTHOR]