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Atrophy of brain structures has been proposed as a biomarker, but it provides little information about biochemical events related to the disease. Here, we propose to identify early and relevant biomarkers by combining biological specificity provided by <jats:sup>1<\/jats:sup>H\u2010MRS and high spatial resolution offered by gluCEST imaging. For this, two different genetic mouse models of Huntington's disease (HD)\u2014the Ki140CAG model, characterized by a slow progression of the disease, and the R6\/1 model, which mimics the juvenile form of HD\u2014were used. Animals were scanned at 11.7 T using a protocol combining <jats:sup>1<\/jats:sup>H\u2010MRS and gluCEST imaging. We measured a significant decrease in levels of N\u2010acetyl\u2010aspartate, a metabolite mainly located in the neuronal compartment, in HD animals, and the decrease seemed to be correlated with disease severity. In addition, variations of tNAA levels were correlated with striatal volumes in both models. Significant variations of glutamate levels were also observed in Ki140CAG but not in R6\/1 mice. Thanks to its high resolution, gluCEST provided complementary insights, and we highlighted alterations in small brain regions such as the corpus callosum in Ki140CAG mice, whereas the glutamate level was unchanged in the whole brain of R6\/1 mice. In this study, we showed that <jats:sup>1<\/jats:sup>H\u2010MRS can provide key information about biological processes occurring in vivo but was limited by the spatial resolution. On the other hand, gluCEST may finely point to alterations in unexpected brain regions, but it can also be blind to disease processes when glutamate levels are preserved. This highlights in a practical context the complementarity of the two methods to study animal models of neurodegenerative diseases and to identify relevant biomarkers.<\/jats:p>","DOI":"10.1002\/nbm.4301","type":"journal-article","created":{"date-parts":[[2020,3,21]],"date-time":"2020-03-21T09:25:54Z","timestamp":1584782754000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":25,"title":["Complementarity of gluCEST and <sup>1<\/sup>H\u2010MRS for the study of mouse models of Huntington's disease"],"prefix":"10.1002","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1650-8899","authenticated-orcid":false,"given":"J\u00e9r\u00e9my","family":"P\u00e9pin","sequence":"first","affiliation":[{"name":"Commissariat \u00e0 l'Energie Atomique (CEA), Direction de la Recherche Fondamentale (DRF), Institut de biologie Fran\u00e7ois Jacob, Molecular Imaging Research Center (MIRCen) Universit\u00e9 Paris\u2010Saclay  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