Assessment of glutamate and glutamine contribution to in vivo N-acetylaspartate quantification in human brain by 1H-magnetic resonance spectroscopy

被引:14
作者
Clementi, V [1 ]
Tonon, C [1 ]
Lodi, R [1 ]
Malucelli, E [1 ]
Barbiroli, B [1 ]
Iotti, S [1 ]
机构
[1] Univ Bologna, Dipartimento Med Clin & Biotecnol Applicata D Cam, Biochim Clin, I-40138 Bologna, Italy
关键词
metabolite quantification; magnetic resonance spectroscopy; hepatic encephalopathy; Glx; N-acetylaspartate;
D O I
10.1002/mrm.20703
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
N-Acetylaspartate (NAA) is one of the most important metabolites detectable by brain H-1-MRS being considered an index of neuronal integrity. At the low magnetic field used in most clinical settings beta,gamma-glutamate/glutamine (GIx) resonances are very close and partially overlap the methyl-NAA resonance interfering with NAA quantification especially at low TE and in the presence of increased GIx signals. NAA overestimation due to Glx on a set of model solutions containing NAA, glutamate, and glutamine in variable amounts was evaluated and the result tested in vivo in six healthy controls and five age- and sex-matched patients with hepatic encephalopathy (HE), the latter having an increased GIx content. A method to assess in vivo the NAA overestimation caused by GIx is proposed. A perfect match was obtained between the assessment of GIx contamination on the NAA of healthy controls and that obtained on the model solutions. However, a substantial difference in NAA overestimation was found between controls and HE patients that cannot be explained by our model. An interpretative hypothesis is provided. Magn Reson Med 54:1333-1339, 2005. (c) 2005 Wiley-Liss, Inc.
引用
收藏
页码:1333 / 1339
页数:7
相关论文
共 39 条
[1]   Mechanisms of hyperammonemia [J].
Bachmann, C .
CLINICAL CHEMISTRY AND LABORATORY MEDICINE, 2002, 40 (07) :653-662
[2]   Abnormal brain energy metabolism shown by in vivo phosphorus magnetic resonance spectroscopy in patients with chronic liver disease [J].
Barbiroli, B ;
Gaiani, S ;
Lodi, R ;
Iotti, S ;
Tonon, C ;
Clementi, V ;
Donati, G ;
Bolondi, L .
BRAIN RESEARCH BULLETIN, 2002, 59 (01) :75-82
[3]   Functions of N-acetyl-L-aspartate and N-acetyl-L-aspartylglutamate in the vertebrate brain:: Role in glial cell-specific signaling [J].
Baslow, MH .
JOURNAL OF NEUROCHEMISTRY, 2000, 75 (02) :453-459
[4]   Preliminary evidence of low cortical GABA levels in localized 1H-MR spectra of alcohol-dependent and hepatic encephalopathy patients [J].
Behar, KL ;
Rothman, DL ;
Petersen, KF ;
Hooten, M ;
Delaney, R ;
Petroff, OAC ;
Shulman, GI ;
Navarro, V ;
Petrakis, IL ;
Charney, DS ;
Krystal, JH .
AMERICAN JOURNAL OF PSYCHIATRY, 1999, 156 (06) :952-954
[5]   Effect of ammonia on GABA uptake and release in cultured astrocytes [J].
Bender, AS ;
Norenberg, MD .
NEUROCHEMISTRY INTERNATIONAL, 2000, 36 (4-5) :389-395
[6]   In vitro expression of N-acetyl aspartate by oligodendrocytes:: Implications for proton magnetic resonance spectroscopy signal in vivo [J].
Bhakoo, KK ;
Pearce, D .
JOURNAL OF NEUROCHEMISTRY, 2000, 74 (01) :254-262
[7]   AMMONIA - KEY FACTOR IN THE PATHOGENESIS OF HEPATIC-ENCEPHALOPATHY [J].
BUTTERWORTH, RF ;
GIGUERE, JF ;
MICHAUD, J ;
LAVOIE, J ;
LAYRARGUES, GP .
NEUROCHEMICAL PATHOLOGY, 1987, 6 (1-2) :1-12
[8]   1H magnetic resonance in the study of hepatic encephalopathy in humans [J].
Córdoba, J ;
Sanpedro, F ;
Alonso, J ;
Rovira, A .
METABOLIC BRAIN DISEASE, 2002, 17 (04) :415-429
[9]  
Danielsen E.R., 1999, MAGNETIC RESONANCE S
[10]   Early N-acetylaspartate depletion is a marker of neuronal dysfunction in rats and primates chronically treated with the mitochondrial toxin 3-nitropropionic acid [J].
Dautry, W ;
Vaufrey, F ;
Brouillet, E ;
Bizat, N ;
Henry, PG ;
Condé, F ;
Bloch, G ;
Hantraye, P .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2000, 20 (05) :789-799