| First Author | Macdonald IR | Year | 2014 |
| Journal | Curr Alzheimer Res | Volume | 11 |
| Issue | 5 | Pages | 450-60 |
| PubMed ID | 24801216 | Mgi Jnum | J:350595 |
| Mgi Id | MGI:7663096 | Doi | 10.2174/1567205011666140505111354 |
| Citation | Macdonald IR, et al. (2014) Early detection of cerebral glucose uptake changes in the 5XFAD mouse. Curr Alzheimer Res 11(5):450-60 |
| abstractText | Brain glucose hypometabolism has been observed in Alzheimer's disease (AD) patients, and is detected with (18)F radiolabelled glucose, using positron emission tomography. A pathological hallmark of AD is deposition of brain beta- amyloid plaques that may influence cerebral glucose metabolism. The five times familial AD (5XFAD) mouse is a model of brain amyloidosis exhibiting AD-like phenotypes. This study examines brain beta-amyloid plaque deposition and (18)FDG uptake, to search for an early biomarker distinguishing 5XFAD from wild-type mice. Thus, brain (18)FDG uptake and plaque deposition was studied in these mice at age 2, 5 and 13 months. The 5XFAD mice demonstrated significantly reduced brain (18)FDG uptake at 13 months relative to wild-type controls but not in younger mice, despite substantial beta- amyloid plaque deposition. However, by comparing the ratio of uptake values for glucose in different regions in the same brain, 5XFAD mice could be distinguished from controls at age 2 months. This method of measuring altered glucose metabolism may represent an early biomarker for the progression of amyloid deposition in the brain. We conclude that brain (18)FDG uptake can be a sensitive biomarker for early detection of abnormal metabolism in the 5XFAD mouse when alternative relative uptake values are utilized. |
