[Abstract Title]. - Society for Neuroscience

CA1. For evaluation of cell survival, the propidium iodide method was applied after 14 days in
vitro.
[Results and Conclusion]
MCTs alone did not maintain the neuronal cell survival. Pyruvate, in the presence of glucose,
showed the protective effects against β-amyloid cell toxicity as well as vitamin E analogue and
nicotinamide. Lactate did not show any protective effects. Pyruvate, but not lactate, also reversed
the β-amyloid induced inhibition of LTP. Pyruvate treatment led to the reduction of the ROS
levels and the increase of the NAD levels in the slices. The involvement of CaMK-II or Protein
Phosphatase-1 with these pyruvate protective actions against β-amyloid in the short term (LTP)
and the long term consequences (cell survival) has been under exploring.
Disclosures: X.N. Wang , None; T. Takata, None; T. Sakurai, None; K. Yokono, None.
Poster
244. Abeta Toxicity I
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 244.8/M1
Topic: C.01.c. Abeta toxicity
Support: MU Research Board Grant URB-04-038
NIH Grant 1P01 AG18357
Alzheimer's Assoiciation Grant NIRG-06-25448
NIH Grant 1R21NS052385
Title: Amyloid-β peptide induces temporal change of astrocytic cell membranes through cPLA2
Authors: *G. Y. SUN 1 , J. HICKS 2 , Y. LAI 2 , W. SHENG 3 , D. ZHU 2 , J. LEE 2 ;
1 Dept Biochem, 2 Dept Biol. Engin., 3 Dept of Pathology and Anatom. Sci., Univ. Missouri,
Columbia, MO
Abstract: Amyloid-beta peptide (Aβ) has been widely implicated as the neurotoxic species in
Alzheimer‟s disease (AD), and has been shown to deposit on cell membranes resulting in
disruption of cell functions. However, mechanisms underlying Aβ‟s effects on cell membranes
have not been fully characterized. In this study, oligomeric amyloid-β1-42 (Aβ42) caused a
temporal biphasic change in astrocytic DITNC cell membranes, where membranes became more
molecularly disordered after ~ 30min-1hr, but more molecularly ordered after ~ 3hr of Aβ42