{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T22:50:34Z","timestamp":1773269434274,"version":"3.50.1"},"reference-count":65,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2012,5,30]],"date-time":"2012-05-30T00:00:00Z","timestamp":1338336000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Movement Disorders"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Huntington's disease (HD) is a neurodegenerative disorder characterized by early cognitive decline that progresses at later stages to dementia and severe movement disorder. HD is caused by a cytosine\u2013adenine\u2013guanine triplet\u2010repeat expansion mutation in the <jats:italic>Huntingtin<\/jats:italic> gene, allowing early diagnosis by genetic testing. This study aimed to identify the relationship of <jats:italic>N<\/jats:italic>\u2010acetylaspartate and other brain metabolites to cognitive function in HD\u2010mutation carriers by using high\u2010field\u2010strength magnetic resonance spectroscopy (MRS) at 7 Tesla. Twelve individuals with the HD mutation in premanifest or early\u2010stage disease versus 12 healthy controls underwent <jats:sup>1<\/jats:sup>H magnetic resonance spectroscopy (7.2 mL voxel in the posterior cingulate cortex) at 7 Tesla, and also T1\u2010weighted structural magnetic resonance imaging. All participants received standardized tests of cognitive functioning including the Montreal Cognitive Assessment and standardized quantified neurological examination within an hour before scanning. Individuals with the HD mutation had significantly lower posterior cingulate cortex <jats:italic>N<\/jats:italic>\u2010acetylaspartate (\u22129.6%, <jats:italic>P<\/jats:italic> = .02) and glutamate (\u221210.1%, <jats:italic>P<\/jats:italic> = .02) levels than did controls. In contrast, in this small group, measures of brain morphology including striatal and ventricle volumes did not differ significantly. Linear regression with Montreal Cognitive Assessment scores revealed significant correlations with <jats:italic>N<\/jats:italic>\u2010acetylaspartate (<jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup> = 0.50, <jats:italic>P<\/jats:italic> = .01) and glutamate (NAA) (<jats:italic>r<\/jats:italic><jats:sup>2<\/jats:sup> = 0.64, <jats:italic>P<\/jats:italic> = .002) in HD subjects. Our data suggest a relationship between reduced <jats:italic>N<\/jats:italic>\u2010acetylaspartate and glutamate levels in the posterior cingulate cortex with cognitive decline in the early stages of HD. <jats:italic>N<\/jats:italic>\u2010acetylaspartate and glutamate magnetic resonance spectroscopy signals of the posterior cingulate cortex region may serve as potential biomarkers of disease progression or treatment outcome in HD and other neurodegenerative disorders with early cognitive dysfunction, when structural brain changes are still minor. \u00a9 2012 Movement Disorder Society<\/jats:p>","DOI":"10.1002\/mds.25010","type":"journal-article","created":{"date-parts":[[2012,5,30]],"date-time":"2012-05-30T11:05:55Z","timestamp":1338375955000},"page":"895-902","source":"Crossref","is-referenced-by-count":66,"title":["Brain metabolite alterations and cognitive dysfunction in early Huntington's disease"],"prefix":"10.1002","volume":"27","author":[{"given":"Paul G.","family":"Unschuld","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard A. 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