Page 106 - ebook

[A. Biochemistry/Molecular Biology] A-53

Traumatic brain injury induces cognitive dysfunction through

the decrease of brain O-GlcNAcylation in zebrafish

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Ngan An Bui¹ , Duong Tran Thi Thuy¹ , Dong Yeol Kim¹, Jiwon Park¹, Sang-Min Kim¹, Hyun Jae Sung¹,
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Quynh Nguyen Thi Nhu¹, Inn Oc Han¹*

¹Biomedical Science and Engineering, Inha University Graduate School, Incheon 22211, Korea

Traumatic brain injury (TBI) is one of the most common neurological disorders, for which the effective therapeutic

methods remain unclear. In this study, we used a novel model of adult zebrafish to search for the underlying
molecular and physiological changes following TBI. Using T-maze, at the 3rd-day post-stab lesion injury (dpi),

learning and memory deficit and poor social response were observed. Results from mirror biting and novel tank
test also provided us insight into their defective mobility, exploration rate, and territorial instincts. Severe brain

inflammation was also observed at 3 dpi. In our previous studies, a decrease of O-GlcNAcylation flux inducing
cognitive impairment was proved, but little is known about whether it applied to the TBI model. Upon injury, a

notable decrease of O-GlcNAc level was remarked at 3dpi. To further investigate this correlation, after TBI exposure,
zebrafish were recovered 3 days in glucosamine (GlcN) diluted in water, which increase O-GlcNAc level. Under the

treatment of GlcN, the inflammation level reduced significantly. TBI-induced O-GlcNAc deficiency, as well as L/M
capability, was also rescued by GlcN. As the result, regulation of brain O-GlcNAcylation may hold a potential role

over TBI’s recuperation.