%0 Journal Article
%T CXB-909 Attenuates Cognitive Deficits in the Mu-P-75 Saporin Mouse Model of Alzheimer¡¯s Disease
%A Steven Lowrance
%A Jessica Matchynski
%A Julien Rossignol
%A Nicholas Dekorver
%A Michael Sandstrom
%A Gary Dunbar
%J Neuroscience & Medicine
%P 65-68
%@ 2158-2947
%D 2012
%I Scientific Research Publishing
%R 10.4236/nm.2012.31010
%X The purpose of this study was to determine if the substituted pyrimidine, CXB-909 (formerly known as KP544) which has been shown to amplify the effects of nerve growth factor in elevating choline-acetyltransferase activity in vitro, could attenuate memory deficits in the mu-p-75 saporin injected mouse model of Alzheimer¡¯s disease (AD). Seventy-one, seven-week old C57/BL6 mice received daily oral intubation of 10, 15, or 20 mg/kg CXB-909, or vehicle (0.5% methylcellulose solution), which continued for 32 days. At postnatal week nine, mice received bilateral intra-cerebroventricular injections of mu-p-75 saporin, or sterile phosphate buffered saline. Seven days after surgery, mice were trained for two days, on a cued-platform version of the Morris water maze task, and then tested on a four-day hidden-platform version, followed by a one-day probe version of this task. Mice injected with mu-p-75 saporin, had increased latency to find the hidden-platform compared to sham mice. Furthermore, mice treated with CXB-909 at the 10, and 15 mg/kg doses, significantly reduced their latency to reach the hidden-platform, compared to vehicle-treated mice given mu-p-75 saporin. These results suggest that CXB-909 can attenuate memory deficits in the mu-p-75 saporin injected mouse model of AD.
%K Alzheimer¡¯s Disease
%K Memory Deficits
%K Substituted Pyrimidines
%K Mu-p-75 Saporin
%K Morris Water Maze
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=17754