[2015 Spring Life Sciences & IBB Regular Seminar]
         
           
       ▶Subject: Neuronal atrophy, in between life and death
         
       ▶Speaker: Prof. Woong Sun 

                      (Department of Anatomy Korea University College of Medicine)
                 
       ▶Date: 4:00PM/May/15(Fri.)/2015
          
       ▶Place: Auditorium(1F), Postech Biotech Center
         
               *Abctract
             Programmed cell death (PCD) of neurons has long been considered to be essential for development and function of nervous system. However, Bax-deleted mice with a complete absence of PCD can form normal neural circuitry and exhibit normal behavior. This surprisingly normal phenotype is due to the compensatory atrophy, i.e. Retraction of the neuronal processes and shrinkage of cell bodies of the surplus neurons. Atrophic changes of neurons were also observed following the blockade of PCD in animal disease models. For example, dopaminergic neurons in Bax-deleted mice were resistant to 6-hydroxydopamine (6-OHDA)-induced neuronal death, and neuronal death was completely blocked. However, those survived DA neurons were markedly atrophied, without any improvements in Parkinson’s disease (PD)-like functions. On the other hand, we found that genetic deletion of Poly [ADP-ribose] polymerase 1 (PARP-1) completely blocked 6-OHDA-induced dopaminergic neurodegeneration and related PD-like symptoms. Hyper-activation of PARP-1 depleted ATP pools in the DA neurons, thereby activated AMP-activated protein kinase (AMPK). Blockade of AMPK activation by viral infection of dominant negative AMPK (DN-AMPK) partially inhibited the DA neuronal degeneration. Collectively, these results suggest that the prevention of neuronal atrophy by manipulation of PARP1-AMPK pathway is an effective therapeutic approach to prevent brain diseases.

       ▶Inquiry: Prof. Park, Sang Ki (279-2349)
               
         
         * This seminar will be given in English.
     please refrain from taking photos during seminars. *