Glutathione relates to neuropsychological functioning in mild cognitive impairment

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dc.contributor.authorDuffy, SLen_AU
dc.contributor.authorLagopoulos, Jen_AU
dc.contributor.authorHickie, IBen_AU
dc.contributor.authorDiamond, Ken_AU
dc.contributor.authorGraeber, MBen_AU
dc.contributor.authorLewis, SJGen_AU
dc.contributor.authorNaismith, SLen_AU
dc.date.accessioned2018-09-16T23:19:26Zen_AU
dc.date.available2018-09-16T23:19:26Zen_AU
dc.date.issued2014-01-01en_AU
dc.date.statistics2018-09-16en_AU
dc.description.abstractBackground Mild cognitive impairment (MCI) represents an at-risk state for Alzheimer's disease in which underlying pathophysiological mechanisms could be delineated. Oxidative stress has been implicated in Alzheimer's disease and can be measured by levels of the antioxidant glutathione. This study aims to assess in vivo levels of glutathione via proton magnetic resonance spectroscopy in patients with MCI and to determine how glutathione relates to cognitive decline. Methods Fifty-four patients with MCI and 41 healthy control subjects underwent proton magnetic resonance spectroscopy in conjunction with medical, psychiatric, and neuropsychological assessments. The concentration of glutathione was measured in the anterior and posterior cingulate, and ratios of glutathione were calculated relative to creatine. Neuropsychological performance was assessed across the domains of processing speed, learning, memory, and executive functions. Results In comparison with control subjects, patients with MCI had significantly elevated ratios of glutathione in the anterior (t = −2.2, P = .03) and posterior (t = −2.9, P = .005) cingulate. Higher levels of anterior cingulate glutathione were related to neuropsychological decrements on tests of executive functions. Elevated posterior cingulate glutathione was associated with poorer memory consolidation. Conclusion This study has shown for the first time that MCI is associated with increased glutathione in the cingulate, which in turn relates to neuropsychological performance. This finding may be indicative of an early compensatory or neuroprotective response, and the role of glial cells and glutathione enzymes requires delineation. Longitudinal studies examining the utility of glutathione as a marker for cognitive decline are now required. © 2014 The Alzheimer's Associationen_AU
dc.identifier.citationDuffy, S. L., Lagopoulos, J., Hickie, I. B., Diamond, K., Graeber, M. B., Lewis, S. J., & Naismith, S. L. (2014). Glutathione relates to neuropsychological functioning in mild cognitive impairment. Alzheimer's & Dementia, 10(1), 67-75. doi:10.1016/j.jalz.2013.01.005en_AU
dc.identifier.govdoc8744en_AU
dc.identifier.issn1552-5260en_AU
dc.identifier.issue1en_AU
dc.identifier.journaltitleAlzheimer's & Dementiaen_AU
dc.identifier.pagination67-75en_AU
dc.identifier.urihttps://doi.org/10.1016/j.jalz.2013.01.005en_AU
dc.identifier.urihttp://apo.ansto.gov.au/dspace/handle/10238/8999en_AU
dc.identifier.volume10en_AU
dc.language.isoenen_AU
dc.publisherElsevieren_AU
dc.subjectGlutathioneen_AU
dc.subjectSpectroscopyen_AU
dc.subjectAtrophyen_AU
dc.subjectNMR spectraen_AU
dc.subjectCerebellumen_AU
dc.subjectBrainen_AU
dc.titleGlutathione relates to neuropsychological functioning in mild cognitive impairmenten_AU
dc.typeJournal Articleen_AU
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