Research Information System
JOURNAL OF KOREAN NEUROSURGICAL SOCIETY, vol.1, no.1, pp.1-2, 2025 (Peer-Reviewed Journal)
| Objective : Alzheimer’s disease is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) peptide aggregation, representing a major therapeutic target. Emerging evidence suggests certain chemotherapeutic agents may attenuate Aβ pathology. Methods : This study investigated the effects of Imatinib, a tyrosine kinase inhibitor with limited blood-brain barrier (BBB) penetration, and Nilotinib, with enhanced BBB permeability, in an intracerebroventricular streptozotocin (ICV-STZ) rat model of Alzheimer’s disease. Outcomes included behavioral assessments (learning latency), hippocampal CA1 and CA3 neuronal counts, and brain concentrations of TNF-α, NF-κB, BDNF, and NRG-1. Results : ICV-STZ administration significantly elevated TNF-α and NF-κB levels and reduced BDNF and NRG-1 expression. Both Imatinib and Nilotinib mitigated these alterations, with Imatinib demonstrating greater efficacy despite its limited BBB permeability. Imatinib and Nilotinib reduced TNF-α and NF-κB levels, increased BDNF and NRG-1 expression, and significantly improved cognitive performance, with latency periods extending from 69.8 seconds in the disease model to 193.5 and 183.1 seconds, respectively. Conclusion : Imatinib and Nilotinib ameliorated neuroinflammation, restored neurotrophic support, and improved cognitive deficits in a preclinical Alzheimer’s disease model. These findings highlight the therapeutic potential of tyrosine kinase inhibitors, warranting further translational research in human studies. |
| Key Words: Alzheimer’s disease · Imatinib · Nilotinib · Neurodegeneration · β-amyloid plaque |