Early regional cerebral glucose hypometabolism in transgenic mice overexpressing the V717F β-amyloid precursor protein

Jean Cosme Dodart, Chantal Mathis, Kelly R. Bales, Steven M. Paul, Arielle Ungerer

Research output: Contribution to journalArticlepeer-review

56 Scopus citations

Abstract

In the present study, we examined whether the relative levels of regional brain [14C]2-deoxyglucose (2-DG) uptake are altered in a transgenic mouse model of Alzheimer's disease which overexpresses a mutated form of the human β-amyloid precursor protein (mutation V717F). We show that the relative levels of 2-DG uptake are significantly reduced in the septum, thalamus, dentate gyrus and parietal cortex of 3-month-old transgenic mice as compared with wild-type littermates. In 10-month-old transgenic mice, these alterations also extend to the CA3 hippocampal region, the cingulate, retrosplenial, occipital and temporal cortices, suggesting an age-dependent decrease in the regional 2-DG uptake. These results suggest that expression of a mutated APP gene induces an early regional cerebral hypometabolism independently of amyloid deposition per se. Copyright (C) 1999 Elsevier Science Ireland Ltd.

Original languageEnglish
Pages (from-to)49-52
Number of pages4
JournalNeuroscience Letters
Volume277
Issue number1
DOIs
StatePublished - Dec 17 1999

Keywords

  • Alzheimer's disease
  • Brain glucose metabolism
  • Transgenic mice
  • [C]2-deoxyglucose
  • β-Amyloid precursor protein

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