Metabolic abnormalities in abstinent methamphetamine dependent subjects

Napapon Sailasuta, Osama Abulseoud, Martha Hernandez, Poone Haghani, Brian D. Ross

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Introduction: Chronic methamphetamine use results in persistent neuropsychological deficits in abstinent methamphetamine dependent (AMD) subjects. We examined the hypothesis that elevated concentration of cerebral glutamate (Glu), an excitatory neurotransmitter and neurotoxin, occurs in human AMD. Materials and Methods: We examined 40 subjects, 18 of whom were AMD, abstinent more than 3 weeks and 22 were age matched controls. A Structured Clinical Interview was applied to exclude AMD with comorbid depression. We used TE-Averaged technique of MRS to uniquely identify and quantify the glutamate resonance at 2.35 ppm on a 3T clinical MR scanner. Statistics, including Bonferroni correction for multiple MRS variables were applied. Results: Glu was significantly higher in frontal white matter of AMD (+19%, P = 0.01) and N-acetylaspartate (NAA), an axonal marker, was lower (-14%, P = 0.004). No significant MRS abnormalities were detected in posterior gray matter. Significant correlations were observed between NAA and Glu (P = 0.002 for AMD and P = 0.06 for controls in the posterior gray matter and P = 0.01 for controls and not significant for AMD in the frontal white matter). Conclusion: Our results demonstrate a significant excess of glutamate in frontal white matter of AMD subjects and offer support for the hypothesis that methamphetamine abuse may exert its long-term neuro-toxicity via glutamate.

Original languageEnglish (US)
Pages (from-to)9-20
Number of pages12
JournalSubstance Abuse: Research and Treatment
Volume4
Issue number1
StatePublished - 2010
Externally publishedYes

Fingerprint

Methamphetamine
Glutamic Acid
Neurotoxins
Neurotransmitter Agents
Interviews

Keywords

  • (3-5) methamphetamine
  • Glutamate
  • Proton MRS
  • TE-average
  • White matter

ASJC Scopus subject areas

  • Psychiatry and Mental health

Cite this

Sailasuta, N., Abulseoud, O., Hernandez, M., Haghani, P., & Ross, B. D. (2010). Metabolic abnormalities in abstinent methamphetamine dependent subjects. Substance Abuse: Research and Treatment, 4(1), 9-20.

Metabolic abnormalities in abstinent methamphetamine dependent subjects. / Sailasuta, Napapon; Abulseoud, Osama; Hernandez, Martha; Haghani, Poone; Ross, Brian D.

In: Substance Abuse: Research and Treatment, Vol. 4, No. 1, 2010, p. 9-20.

Research output: Contribution to journalArticle

Sailasuta, N, Abulseoud, O, Hernandez, M, Haghani, P & Ross, BD 2010, 'Metabolic abnormalities in abstinent methamphetamine dependent subjects', Substance Abuse: Research and Treatment, vol. 4, no. 1, pp. 9-20.
Sailasuta N, Abulseoud O, Hernandez M, Haghani P, Ross BD. Metabolic abnormalities in abstinent methamphetamine dependent subjects. Substance Abuse: Research and Treatment. 2010;4(1):9-20.
Sailasuta, Napapon ; Abulseoud, Osama ; Hernandez, Martha ; Haghani, Poone ; Ross, Brian D. / Metabolic abnormalities in abstinent methamphetamine dependent subjects. In: Substance Abuse: Research and Treatment. 2010 ; Vol. 4, No. 1. pp. 9-20.
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N2 - Introduction: Chronic methamphetamine use results in persistent neuropsychological deficits in abstinent methamphetamine dependent (AMD) subjects. We examined the hypothesis that elevated concentration of cerebral glutamate (Glu), an excitatory neurotransmitter and neurotoxin, occurs in human AMD. Materials and Methods: We examined 40 subjects, 18 of whom were AMD, abstinent more than 3 weeks and 22 were age matched controls. A Structured Clinical Interview was applied to exclude AMD with comorbid depression. We used TE-Averaged technique of MRS to uniquely identify and quantify the glutamate resonance at 2.35 ppm on a 3T clinical MR scanner. Statistics, including Bonferroni correction for multiple MRS variables were applied. Results: Glu was significantly higher in frontal white matter of AMD (+19%, P = 0.01) and N-acetylaspartate (NAA), an axonal marker, was lower (-14%, P = 0.004). No significant MRS abnormalities were detected in posterior gray matter. Significant correlations were observed between NAA and Glu (P = 0.002 for AMD and P = 0.06 for controls in the posterior gray matter and P = 0.01 for controls and not significant for AMD in the frontal white matter). Conclusion: Our results demonstrate a significant excess of glutamate in frontal white matter of AMD subjects and offer support for the hypothesis that methamphetamine abuse may exert its long-term neuro-toxicity via glutamate.

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