me neither. the top results on google scholar show studies that did look at it, but the significant findings involved other variables, ie NAA:creatine ratio is lower in MS.
two abstracts:
http://www.ncbi.nlm.nih.gov/pubmed/1324631
Multiple sclerosis in children: Cerebral metabolic alterations monitored by localized proton magnetic resonance spectroscopy in vivo
Abstract
In vivo proton magnetic resonance spectroscopy of 8 children (7-16 years) with established multiple sclerosis revealed distinct alterations in regional cerebral metabolism associated with different aspects of the disease: (1) Localized proton spectra (2 to 4-ml volumes of interest) from multiple sclerosis plaques were generally characterized by a decrease in N-acetylaspartate and creatines, and an increase in cholines and myo-inositol relative to age-matched control subjects,
(2) neither chronic nor enhancing plaques (by gadolinium-diethylenetriamine pentaacetic acid) during an acute exacerbation showed elevated levels of lactate or lipids, (3) spectra from adjacent white matter that did not appear suspicious in magnetic resonance images were similar to those of normal control subjects, and
(4) cortical gray matter related to neighboring multiple sclerosis lesions showed a notable reduction of N-acetylaspartate. The present results show that functional impairment in multiple sclerosis is linked to gross metabolic disturbances of neuronal cell chemistry. We suggest that focal demyelination is accompanied by increased membrane precursors of proliferative turnover and is associated with secondary neuronal shrinkage or loss, perhaps extending into related cortical gray matter.
http://www3.interscience.wiley.com/jour ... 9/abstract
Zinc deficiency and oxidative stress in brain: Magnetic resonance investigations in weanling rats
Abstract
In humans, zinc deficiency is characterized by a broad spectrum of neurological clinical syndromes. It is known that vesicular zinc-enriched areas of the brain, such as the hippocampus, are responsive to zinc deprivation, which may result in learning impairment. Recent findings show that zinc deficiency may cause alterations in neurochemical activity. In this study we used contrast-enhanced magnetic resonance imaging (MRI) to monitor disruptions to the blood-brain barrier (BBB) and image-guided MR spectroscopy to follow alterations in brain metabolites as a result of zinc-deficiency and/or hyperoxia-induced oxidative stress. Gadolinium-diethylaminetriaminopentaacetic acid, an extracellular T1 relaxation contrast agent, increases tissue water signal in the brain if the BBB is damaged. A
significant increase in postcontrast T1-weighted MR image
intensity was observed in the brain of zinc-deficient or hyperoxia-exposed rats, as well as zinc-deficient rats exposed only to hyperoxia when compared with zinc-adequate rats. From single-voxel image-guided MR spectroscopy results,
significant decreases in the ratio of N-acetyl aspartate, a neuronal-specific compound,
to total choline levels were found when comparing controls (zinc-adequate or zinc pair-fed) with zinc-deficiency or hyperoxia groups alone, and when zinc-deficiency was combined with hyperoxia. This study demonstrates the sensitivity of MR techniques in the ability to monitor the effect of zinc deficiency combined with oxidative stress on BBB permeability as well as detect alterations in brain metabolites. This will further aid in our understanding of the possible cellular and molecular mechanisms involved in zinc deficiency pathology associated with the brain.
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