Literature DB >> 17693392

Brain metabolite abnormalities in the white matter of elderly schizophrenic subjects: implication for glial dysfunction.

Linda Chang1, Joseph Friedman, Thomas Ernst, Kai Zhong, Nicholas D Tsopelas, Kenneth Davis.   

Abstract

BACKGROUND: Abnormalities in the white matter of the brain may occur in individuals with schizophrenia as well as with normal aging. Therefore, elderly schizophrenic patients may suffer further cognitive decline as they age. This study determined whether elderly schizophrenia participants, especially those with declined cognitive function (Clinical Dementia Rating score > 1), show white matter metabolite abnormalities on proton magnetic resonance spectroscopy and whether there are group differences in age-dependent changes in these brain metabolites.
METHOD: Twenty-three elderly schizophrenia and twenty-two comparison participants fulfilling study criteria were enrolled. Localized, short echo-time (1)H MRS at 4 Tesla was used to assess neurometabolite concentrations in several white matter regions.
RESULTS: Compared with healthy subjects, schizophrenia participants had lower N-acetyl compounds (-12.6%, p = .0008), lower myo-inositol (-16.4%, p = .026), and higher glutamate + glutamine (+28.7%, p = .0016) concentrations across brain regions. Schizophrenia participants with Clinical Dementia Rating >/= 1 showed the lowest NA in the frontal and temporal regions compared with control subjects. Interactions between age and schizophrenia status on total creatine and choline-containing compounds were observed; only schizophrenia participants showed age-related decreases of these metabolites in the right frontal region.
CONCLUSIONS: Decreased NA in these white matter brain regions likely reflects reduced neuronal content associated with decreased synapses and neuronal cell volumes. The elevated glutamate + glutamine, if reflecting elevated glutamate, could result from excess neuronal glutamate release or glial dysfunction in glutamate reuptake. The decreased myo-inositol in participants with schizophrenia suggests decreased glial content or dysfunctional glia, which might result from glutamate-mediated toxicity.

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Year:  2007        PMID: 17693392      PMCID: PMC2222890          DOI: 10.1016/j.biopsych.2007.05.025

Source DB:  PubMed          Journal:  Biol Psychiatry        ISSN: 0006-3223            Impact factor:   13.382


  61 in total

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4.  Long-term treatment of rats with haloperidol: lack of an effect on brain N-acetyl aspartate levels.

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5.  Executive function and cognitive subprocesses in first-episode, drug-naive schizophrenia: an analysis of N-back performance.

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  44 in total

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2.  Tract-based magnetic resonance spectroscopy of the cingulum bundles at 7 T.

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Review 4.  Glutamatergic abnormalities in schizophrenia: a review of proton MRS findings.

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Review 6.  Glutamate in schizophrenia: a focused review and meta-analysis of ¹H-MRS studies.

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8.  Elevated Myo-Inositol, Choline, and Glutamate Levels in the Associative Striatum of Antipsychotic-Naive Patients With First-Episode Psychosis: A Proton Magnetic Resonance Spectroscopy Study With Implications for Glial Dysfunction.

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9.  Glutamate levels in the associative striatum before and after 4 weeks of antipsychotic treatment in first-episode psychosis: a longitudinal proton magnetic resonance spectroscopy study.

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10.  Cross-sectional Study of Glutamate in the Anterior Cingulate and Hippocampus in Schizophrenia.

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