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[Q. Neuroscience-51]



                      Repetitive head injury alters olfactory-associated


                   electroencephalographic, behavioral and pathological


                                               sequelae in mice



          Younghyun Yoon¹˙²˙#, YunHee Seol¹˙#, Hyoenjoo Im¹, Hyun Soo Shim¹, Hio-Been Han¹˙³, Jeongeun Kum¹˙⁴,

                                            Jee Hyun Choi¹˙⁴˙*, Hoon Ryu¹˙⁵˙*


         ¹Center for Neuroscience, Korea Institute of Science and Technology, Seoul 02792, ROK, ²Department of Electrical

         Engineering and Computer Science, Vanderbilt University, Nashville 37235, USA, ³Program of Brain and Cognitive
           Engineering, Korea Institute of Science and Technology, Daejeon 34141, ROK, ⁴Department of Neuroscience,
         Division of Bio-Medical Science & Technology, Seoul 02792, ROK, ⁵Boston University Alzheimer’s Disease Center

                    and Department of Neurology, Boston University School of Medicine, Boston 02130, USA




        A series of repeated mild traumatic brain injury (TBI) by collision sports or accidents lead to long-term cognitive

        impairments with an increased risk for neurodegenerative and psychiatric disorders. Olfactory dysfunction has been
        observed as one of the most prominent symptoms in TBI patients, but the exact pathological mechanism is not

        fully understood. In this present study, we investigated the acute effects of repetitive TBI on olfactory functioning
        and  its  pathological  neuronal  injuries using  a TBI mouse model  that  mimics  concussions  in  humans.

        Electroencephalography (EEG) neural impairments were observed in the olfactory bulb. Modulation index values for
        delta-phase  were  significantly  attenuated  in  fast  oscillations  in  concussed  mice  and  cross-frequency  couplings

        between  delta  phase  and  beta/low  gamma  amplitude  were  also  significantly  reduced.  Through  pathological
        examination, we found a significant increase in p-Tau (S202/T205) in olfactory bulb-associated areas. Furthermore,
        neuronal atrophy was correlated with p-Tau level. Lastly, TBI mice showed for an abnormal loss of preference in

        home bedding under Y-maze conditions compared to controls. Together, p-Tau alterations may serve as important

        biomarkers of olfactory track-associated dysfunctions and behavioral impairments
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