ArticleNoro psikiyatri arsivi2023
The Effect of Lidocaine on the Experimental Model of Streptozotocin-Induced Alzheimer's Disease.
Article in Noro psikiyatri arsivi, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Precision Drug Repurposing (PDR): Patient-level modeling and prediction combining foundational knowledge graph with biobank data.Journal of biomedical informatics · 2025Article
- Zhinao Capsule Improved Sleep and Memory Disorders in APP/PS1 Mice via cAMP/PKA/CREB Signaling Pathway Modulation.Drug design, development and therapy · 2025Article
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8 authors.
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Abstract
Introduction: Alzheimer's disease (AD) is a neurodegenerative disease caused by the accumulation of amyloid plaques in the cerebral cortex and hippocampus. In this study, the effects of local anesthetic lidocaine on neurodegeneration markers and memory were investigated for the first time in streptozotocin-induced rat AD model. Methods: Streptozotocin (STZ) was administered intracerebroventricularly (ICV) into Wistar rats to develop AD model. For lidocaine group (n=14), lidocaine (5 mg/kg) was administered intraperitoneally (IP) in addition to STZ injection. Control group animals (n=9) were treated with saline for 21 days. Morris Water Maze (MWM) test was performed to evaluate memory after the injections were completed. Also, the serum levels of TAR DNA-binding protein-43 (TDP-43), amyloid precursor protein (APP), β-secretase 1, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), response element binding protein (CREB), c-FOS were measured using ELISA test and compared between groups. Results: Lidocaine group animals showed lower escape latency and time in quadrant scores in MWM inferring better memory performance. Furthermore, lidocaine administration caused a significant decline in TDP-43 levels. However, the expression of APP and β-secretase were significantly higher in AD and lidocaine groups compared to control group. Moreover, lidocaine group markedly had higher serum NGF, BDNF, CREB, and c-FOS levels compared to those in the AD group. Conclusion: In addition to neuroprotective effects in STZ-induced AD model, Lidocaine also appears to improve memory. This effect might be associated with increased levels of several growth factors and associated intracellular molecules. The therapeutic role of lidocaine in the pathophysiology of AD should be studied in the future.
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