@inproceedings{oai:repo.qst.go.jp:00054486,
 author = {Takanashi, Junichi and Saito, Shigeyoshi and Aoki, Ichio and J., Barkovich A. and Terada, H. and Ito, Y. and Inoue, K. and 高梨 潤一 and 齋藤 茂芳 and 青木 伊知男},
 book = {Proc. Intl. Soc. Mag. Reson. Med.},
 month = {May},
 note = {N-acetylaspartate (NAA) is a compound found predominantly in neurons and their processes, and is generally considered to be an important marker of viable, functioning neurons and axons. Many neurodegenerative disorders, therefore, exhibit a decrease of total NAA (tNAA; NAA at 2.01 ppm and N-acetylaspartylglutamate [NAAG] at 2.04 ppm, which are difficult to distinguish on clinical 1H-MRS with a 1.5 or 3.0 tesla magnet). Previous studies have shown the elevation of tNAA on 1H-MRS with 1.5 tesla magnet in Pelizaeus-Merbacher disease (PMD), a representative hypomyelination disease. In order to evaluate a hypothesis that hypomyelinating process may affect NAA and NAAG biochemical pathways, we examined myelin synthesis-deficient (msd) mouse brain, a model of PMD with a 7.0 tesla magnet and separately measured NAA and NAAG of the brains of these animals by high performance liquid chromatography (HPLC).},
 pages = {4181--4181},
 title = {Brain N-Acetylaspartate Is Increased in Mice with Hypomyelination},
 volume = {19},
 year = {2011}
}