An integrated strategy for evaluation of metabolic and oxidative defects in neurodegenerative illness using magnetic resonance techniques

被引:13
作者
Jenkins, BG
Chen, YI
Kuestermann, E
Makris, NM
Nguyen, TV
Kraft, E
Brownell, AL
Rosas, HD
Kennedy, DN
Rosen, BR
Koroshetz, WJ
Beal, MF
机构
[1] Massachusetts Gen Hosp, NMR Ctr, Dept Radiol, Charlestown, MA 02129 USA
[2] Harvard Univ, Sch Med, Charlestown, MA 02129 USA
来源
OXIDATIVE/ENERGY METABOLISM IN NEURODEGENERATIVE DISORDERS | 1999年 / 893卷
关键词
D O I
10.1111/j.1749-6632.1999.tb07828.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The number of physiologic and metabolic phenomena amenable to analysis using magnetic resonance (MR) techniques is increasing every year. MR techniques tan now evalutate tissue parameters relevant to TCA. cyclemetabolism, anerobic glycolysis, ATP levels, blood-brain barrier permeability, macrophage infiltration, cytotoxic edema, spreading depression, cerebral blood now and volume, and neurotransmitter function. The paramagnetic nature of certain oxidation states of iron leads to the ability to map out brain function using deoxyhemoglobin as an endogenous contrast agent, and also allows for mapping of local tissue iran concentrations. Zn addtion to these metabolic parameters, the number of ways to generate anatomic contrast using MR is also expanding; and In addition to conventional anatomic scans, mapping of axonal fiber tracts can also be performed using the anisotropy of eater diffusion, rt strategy for integration of these multifarious parameters in a comprehensive neurofunctional exam in neurodegenerative illness is outlined in this paper. The goals of the integrated exam, as applied to a given neurodegenerative illness, can be subdivided into three categories: etiology, natural history, and therapeutic end points, The consequences of oxidative stress and/or mitochondrial dysfunction are explored in the contest of the various parameters that can be measured using the integrated MR exam.
引用
收藏
页码:214 / 242
页数:29
相关论文
共 146 条
[1]   Striatal glucose metabolism and dopamine D-2 receptor binding in asymptomatic gene carriers and patients with Huntington's disease [J].
Antonini, A ;
Leenders, KL ;
Spiegel, R ;
Meier, D ;
Vontobel, P ;
WeigellWeber, M ;
SanchezPernaute, R ;
deYebenez, JG ;
Boesiger, P ;
Weindl, A ;
Maguire, RP .
BRAIN, 1996, 119 :2085-2095
[2]   T2 RELAXATION-TIME IN PATIENTS WITH PARKINSONS-DISEASE [J].
ANTONINI, A ;
LEENDERS, KL ;
MEIER, D ;
OERTEL, WH ;
BOESIGER, P ;
ANLIKER, M .
NEUROLOGY, 1993, 43 (04) :697-700
[3]   DEFECTIVE BRAIN ENERGY-METABOLISM SHOWN BY INVIVO P-31 MR SPECTROSCOPY IN 28 PATIENTS WITH MITOCHONDRIAL CYTOPATHIES [J].
BARBIROLI, B ;
MONTAGNA, P ;
MARTINELLI, P ;
LODI, R ;
IOTTI, S ;
CORTELLI, P ;
FUNICELLO, R ;
ZANIOL, P .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1993, 13 (03) :469-474
[4]   Aspects of human bioenergetics as studied in vivo by magnetic resonance spectroscopy [J].
Barbiroli, B ;
Iotti, S ;
Lodi, R .
BIOCHIMIE, 1998, 80 (10) :847-853
[5]   RATES OF DECREASE OF CEREBRAL BLOOD-FLOW IN PROGRESSIVE DEMENTIAS [J].
BARCLAY, L ;
ZEMCOV, A ;
BLASS, JP ;
MCDOWELL, F .
NEUROLOGY, 1984, 34 (12) :1555-1560
[6]   MR DIFFUSION TENSOR SPECTROSCOPY AND IMAGING [J].
BASSER, PJ ;
MATTIELLO, J ;
LEBIHAN, D .
BIOPHYSICAL JOURNAL, 1994, 66 (01) :259-267
[7]  
Basser PJ, 1996, J MAGN RESON SER B, V111, P209, DOI [10.1006/jmrb.1996.0086, 10.1016/j.jmr.2011.09.022]
[8]   Inhibition of N-acetylaspartate production: Implications for H-1 MRS studies in vivo [J].
Bates, TE ;
Strangward, M ;
Keelan, J ;
Davey, GP ;
Munro, PMG ;
Clark, JB .
NEUROREPORT, 1996, 7 (08) :1397-1400
[9]   AGING, ENERGY, AND OXIDATIVE STRESS IN NEURODEGENERATIVE DISEASES [J].
BEAL, MF .
ANNALS OF NEUROLOGY, 1995, 38 (03) :357-366
[10]   Mitochondrial Dysfunction in Neurodegenerative Diseases [J].
Johri, Ashu ;
Beal, M. Flint .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2012, 342 (03) :619-630