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Magnetic resonance spectroscopy (<jats:styled-content style=\"fixed-case\">MRS<\/jats:styled-content>) has been touted as a suitable method for discriminating<jats:italic>in vivo<\/jats:italic>markers of neuroinflammation. The present<jats:styled-content style=\"fixed-case\">MRS<\/jats:styled-content>study was conducted in four groups: alcohol dependent (<jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>, n\u2009=\u200937),<jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>\u2010infected (<jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>, n\u2009=\u200933), alcohol dependent\u2009+\u2009<jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>infected (<jats:styled-content style=\"fixed-case\">HA<\/jats:styled-content>, n\u2009=\u200938) and healthy control (<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>, n\u2009=\u200962) individuals to determine whether metabolites would change in a pattern reflecting neuroinflammation. Significant four\u2010group comparisons were evident only for striatal choline\u2010containing compounds (<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>ho) and myo\u2010inositol (<jats:styled-content style=\"fixed-case\">mI<\/jats:styled-content>), which follow\u2010up analysis demonstrated were due to higher levels in<jats:styled-content style=\"fixed-case\">HA<\/jats:styled-content>compared with<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>individuals. To explore the potential relevance of elevated<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>ho and<jats:styled-content style=\"fixed-case\">mI<\/jats:styled-content>, correlations between blood markers, medication status and alcohol consumption were evaluated in<jats:styled-content style=\"fixed-case\">H<\/jats:styled-content>\u2009+\u2009<jats:styled-content style=\"fixed-case\">HA<\/jats:styled-content>subjects. Having an acquired immune deficiency syndrome (<jats:styled-content style=\"fixed-case\">AIDS<\/jats:styled-content>)\u2010defining event or hepatitis<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>was associated with higher<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>ho; lower<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>ho levels, however, were associated with low thiamine levels and with highly active antiretroviral<jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>treatment (<jats:styled-content style=\"fixed-case\">HAART<\/jats:styled-content>). Higher levels of<jats:styled-content style=\"fixed-case\">mI<\/jats:styled-content>were related to greater lifetime alcohol consumed, whereas<jats:styled-content style=\"fixed-case\">HAART<\/jats:styled-content>was associated with lower<jats:styled-content style=\"fixed-case\">mI<\/jats:styled-content>levels. The current results suggest that competing mechanisms can influence<jats:italic>in vivo<\/jats:italic>\u2005<jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>ho and<jats:styled-content style=\"fixed-case\">mI<\/jats:styled-content>levels, and that elevations in these metabolites cannot necessarily be interpreted as reflecting a single underlying mechanism, including neuroinflammation.<\/jats:p>","DOI":"10.1111\/bpa.12197","type":"journal-article","created":{"date-parts":[[2014,10,27]],"date-time":"2014-10-27T02:15:04Z","timestamp":1414376104000},"page":"654-664","source":"Crossref","is-referenced-by-count":60,"title":["Imaging Neuroinflammation? 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