• Alpaslan Dedeoglu, Ji-Kyung Choi, Kerry Cormier, Neil W Kowall, and Bruce G Jenkins.
• Geriatric Research Education and Clinical Center, Bedford Veterans Administration Medical Center, MA 01730, USA. dedeoglu@bu.edu
• Brain Res. 2004 Jun 25;1012(1-2):60-5.

AbstractTransgenic mice that express mutant human amyloid precursor protein (APPTg2576) develop beta-amyloid (Abeta) plaques throughout the cortex starting at 10-12 months of age. We examined the neurochemical profile of APPTg2576 mice using in vitro and in vivo magnetic resonance spectroscopy (MRS); gross abnormalities using magnetic resonance imaging (MRI) and plaque distribution; size and number using immunohistochemistry. Transgenic mice were anesthetized with halothane and scanned at 4.7 T using T2-weighted imaging and in vivo MRS of frontal cortex. In vitro MRS was run from brain extracts of frontal cortex in both APP and wild-type mice. Mice were also perfused and brains were collected and cut for immunohistochemistry. We found that N-acetylaspartate (NAA), glutamate and glutathione were decreased by 17%, 22% and 36%, respectively, in the cerebral cortex of APP transgenic mice at 19 months of age when Abeta deposits are widespread. Taurine was increased 21% compared to wild-type. Decreased levels of NAA and increased levels of taurine are consistent with decreased neuronal viability and increased glial volume, and are similar to findings of decreased NAA and increased myo-inositol in human Alzheimer's disease (AD) brains. Correlation between the severity of Abeta deposition and altered neurochemical profile remains to be studied. Nevertheless, the altered neurochemical profile may be a valuable marker to test therapeutics in this mouse model.Copyright 2004 Elsevier B.V.

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