Role of phospholipase A2 on the variations of the choline signal intensity observed by 1H magnetic resonance spectroscopy in brain diseases11Published on the World Wide Web on 10 August 2000.

Boulanger, Yvan; Labelle, Martin; Khiat, Abdesslem

doi:10.1016/s0165-0173(00)00037-0

Cited by 81 publications

(51 citation statements)

References 95 publications

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“…The Cho signal is mainly derived from the precursors of phosphatidylcholine, phosphocholine, free choline, and glycerophosphocholine. 21 Overall, our results are in agreement with the recent estimation on the methyl group balance in humans. 19,20 Phosphatidylethanolamine methyltransferase is the rate-limiting step of phosphatidylcholine synthesis in the liver.…”

Section: Figure 2 Scatter Plots Of the Choline/creatine Ratio Accordisupporting

confidence: 92%

Reduced brain choline in homocystinuria due to remethylation defects

Debray¹,

Boulanger²,

Khiat³

et al. 2008

Neurology

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Reduced brain choline in homocystinuria due to remethylation defects This information is current as of January 30, 2009http://www.neurology.org/cgi/content/full/71/1/44 located on the World Wide Web at:The online version of this article, along with updated information and services, is Objective:To investigate whether secondary impairment of the transmethylation pathway is a mechanism underlying the neurologic involvement in homocystinuria due to remethylation defects.Methods: Twelve patients with neurologic disease due to remethylation defects were examined by brain magnetic resonance spectroscopic imaging ( 1 H MRSI). Brain N-acetylaspartate, cholinecontaining compounds (Cho), and creatine (Cr) were quantified and compared to with controls. Metabolites of remethylation cycle and creatine biosynthesis pathway were measured in plasma and urine.Results: MRSI revealed isolated Cho deficiency in all regions examined (mean concentration units Ϯ SD, patients vs controls): frontal white matter (0.051 Ϯ 0.010 vs 0.064 Ϯ 0.010; p ϭ 0.001), lenticular nucleus (0.056 Ϯ 0.011 vs 0.069 Ϯ 0.009; p Ͻ 0.001), and thalamus (0.063 Ϯ 0.010 vs 0.071 Ϯ 0.007; p ϭ 0.006). In contrast to controls, the Cho/Cr ratio decreased with age in patients in the three brain regions examined. Low creatine urinary excretion (p Ͻ 0.005), normal urine and plasma guanidinoacetate, and a paradoxical increase in plasma S-adenosylmethionine (p Ͻ 0.005) concentrations were observed. Conclusion:Patients with homocystinuria due to remethylation defects have an isolated brain choline deficiency, probably secondary to depletion of labile methyl groups produced by the transmethylation pathway. Although biochemical studies suggest mild peripheral creatine deficiency, brain creatine is in the reference range, indicating a possible compartmentation phenomenon. Paradoxical increase of S-adenosylmethionine suggests that secondary inhibition of methylases contributes to the transmethylation defect in these conditions. Neurology GLOSSARYCblC ϭ combined homocystinuria-methylmalonic aciduria; CblG ϭ methionine synthase deficiency; CBS ϭ cystathionine ␤-synthase; Cho ϭ water-soluble choline-containing compounds; Cr ϭ creatine; DQ ϭ developmental quotient; Met ϭ plasma methionine; MR ϭ magnetic resonance; MSRI ϭ magnetic resonance spectroscopic imaging; MTHFR ϭ methylene tetrahydrofolate reductase; NA ϭ not available; NAA ϭ N-acetylaspartate; NN ϭ neonatal; NS ϭ not significant; OA ϭ optic atrophy; OMA ϭ oculomotor apraxia; OMIM ϭ Online Mendelian Inheritance in Man; PM ϭ pigmentary maculopathy; Pt ϭ patient; RD ϭ remethylation defect; RP ϭ retinitis pigmentosa; tHcy ϭ plasma total homocysteine; THF ϭ tetrahydrofolate.

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Section: Figure 2 Scatter Plots Of the Choline/creatine Ratio Accordisupporting

confidence: 92%

Reduced brain choline in homocystinuria due to remethylation defects

Debray¹,

Boulanger²,

Khiat³

et al. 2008

Neurology

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“…The main contributors to the choline resonance in brain are glycerophosphocholine and phosphocholine, 2 intermediates of the phosphatidylcholine pathway. 45 Their increase has essentially been reported in brain tumors and diseases characterized by myelin alterations. [45][46][47] The abnormal ADC value in the parietal white matter together with the increase in Cho/H 2 O and mIns/H 2 O in the centrum semiovale indicate the existence of subtle white matter injury and gliosis not visible by conventional MR imaging.…”

Section: Discussionmentioning

confidence: 98%

Is Brain Maturation Comparable in Fetuses and Premature Neonates at Term Equivalent Age?

Viola

Confort‐Gouny²,

Schneider³

et al. 2011

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:Improved knowledge of brain maturation in fetuses and premature neonates is crucial for the early detection of pathologies and would help determine whether MR data from the premature brain might be used to evaluate fetal maturation. Using diffusion-weighted MR imaging and 1 H-MR spectroscopy, we compared cerebral microstructure and metabolism in normal in utero fetuses imaged near term and premature neonates imaged at term equivalent.

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“…N-acetylaspartate has been described as a sensitive marker of neuronal functionality/viability, 10 and defects on that signal could reflect damage or loss of neurons, reductions of interneuronal neuropil, neuronal or axonal metabolic dysfunction or some combination of these processes. 29 Reductions of NAA have been observed in patients with bipolar 30 and pediatric depression, 31 but there is no consistent agreement for altered NAA levels in the hippocampus in previous MRS studies of adult unipolar depression.…”

Section: Discussionmentioning

confidence: 99%

“…9 Resonance of Cho can be conceived as an indirect measure of membrane turnover. 10 Primarily present in neurons, NAA is suggested to be a marker of neuronal viability and functionality. 11 In last decade, a large and compelling body of literature on biochemical changes in MDD has appeared, but only a few works have focused on the hippocampus, sometimes leading to inconsistent conclusions.…”

Section: Introductionmentioning

confidence: 99%