central-nervous-system-2016_posters-accepted-abstracts

14 / 42

Notes:
Page 70
CNS 2016
December 05-07, 2016
Volume 7, Issue 5(Suppl) J Neurol Neurophysiol
ISSN: 2155-9562 JNN, an open access journal
conferenceseries .com
December 05-07, 2016 Dubai, UAE
2nd International Conference on
Central Nervous System Disorders & Therapeutics
Melanie Tepper, J Neurol Neurophysiol 2016, 7:5(Suppl)
Consequences of neuron-specific NF κB modulation on the outcome of traumatic brain injury
Melanie Tepper
Institute of Physiological Chemistry, Ulm University, Germany
The outcome of traumatic brain injury (TBI) greatly depends on the extent of secondary pathologies.This posttraumatic phase
is characterized by diverse cellular events including neuroinflammation, apoptosis and necrosis as well as counteracting
regeneration and remodeling processes. IKK/NF κB signaling is a key player in the regulation of inflammation, immune
responses, cell survival and neuronal differentiation and is known to get activated in different cell types of the CNS upon TBI.
However, the cell-type-specific functions of NF κB remain unclear. We therefore conducted a systematic approach to analyze
whether IKK/NF κB signaling has either beneficial or detrimental effects on the outcome of TBI depending on the cell type.
For this purpose, we used an experimental model of closed head injury in combination with either loss-of-function or gain-
of-function mice allowing conditional inhibition or activation of NF κB in principal forebrain neurons. Outcome parameters
consisted of in vivo neurological scoring as well as post mortem investigation of inflammatory, apoptotic and synaptic markers.
We provide evidence that repression of IKK/NF κB signaling in neurons increases the acute posttraumatic mortality rate and
worsens the neurological outcome of survivors at various time points post TBI. Interestingly, IKK2 DNCamk2a mice are
more prone for hematoma formation and show increased neuroinflammation, reactive astrogliosis and alterations in gene
expression. These findings suggest that neuronal NF κB inhibition plays a detrimental role for the outcome of TBI. Currently
we investigate whether enhancing neuronal NF κB activation can reduce these harmful effects of secondary TBI pathogenesis.
This study is supported by the German Research Foundation (SFB 1149/A03).
Biography
Melanie Tepper has completed her Bachelor studies in Molecular Biotechnology at the University of Heidelberg, Germany. Afterwards she had the chance to study
one year at the San Francisco State University, CA, USA as a Fulbright student in Cell and Molecular Biology and finished her Master Studies in Molecular Medicine
at Ulm University, Germany. She is currently in her 3rd year as a PhD student from the International Graduate School Ulm in the group of Prof. Dr. Thomas Wirth
and Dr. Bernd Baumann.