목적: Traumatic brain injury (TBI) is a major cause of olfactory dysfunction, significantly affecting patients' quality of life. Among the underlying pathological mechanisms, Wallerian degeneration plays a critical role in axonal disruption within the olfactory pathway. This study investigates the relationship between Wallerian degeneration and post-TBI olfactory dysfunction using a TBI-induce anosmia mouse model. 방법:Anosmia was induced through bilateral olfactory bulbectomy to examine the progression of Wallerian degeneration within the olfactory pathways. Olfactory function was evaluated through behavioral odor test, while histological and immunohistochemical analyses assessed axonal degeneration. Markers such as Nicotinamide Mononucleotide Adenylyltransferase 2 (NMNAT2) and Sterile Alpha and TIR Motif- Containing 1 (SARM1), S100β, Myelin Basic Protein (MBP), neurofilament, βIII-Tubulin (Tuj1) and olfactory, Olfactory Marker Protein (OMP) were used to assess axonal degeneration and olfactory sensory neurons. 결과:Behavioral olfactory function test confirmed sensory deficits post-TBI. Histological analyses revealed progressive Wallerian degeneration in the olfactory epithelium characterized by disrupted axonal architecture, reduced Tuj1 and OMP expression, decreased expression of NMMNAT2 and increased SARM1 activation. 결론:Our findings indicate that TBI induces progressive Wallerian degeneration, contributing to olfactory impairment. Understanding the role of Wallerian degeneration in TBI-induced anosmia may offer new therapeutic targets for sensory restoration in affected individuals