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Publication : Early regional cerebral glucose hypometabolism in transgenic mice overexpressing the V717F beta-amyloid precursor protein.

First Author  Dodart JC Year  1999
Journal  Neurosci Lett Volume  277
Issue  1 Pages  49-52
PubMed ID  10643895 Mgi Jnum  J:60044
Mgi Id  MGI:1352566 Doi  10.1016/s0304-3940(99)00847-2
Citation  Dodart JC, et al. (1999) Early regional cerebral glucose hypometabolism in transgenic mice overexpressing the V717F beta-amyloid precursor protein. Neurosci Lett 277(1):49-52
abstractText  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 beta-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.
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