Cortical glucose metabolism is altered in aged transgenic Tg2576 mice that demonstrate Alzheimer plaque pathology.

摘要: Alzheimer's disease is associated with markedly impaired cerebral glucose metabolism as detected by reduced cortical desoxyglucose utilization, altered activities of key glycolytic enzymes or densities transporter subtypes. To determine whether formation and/or deposition β-amyloid plays a role in the pathology metabolism, transgenic Tg2576 mice that overexpress Swedish mutation human amyloid precursor protein and demonstrate progressive, age-related hippocampal plaques, were used to study expression activity brain glycolysis (phosphofructokinase, PFK) glyconeogenesis (fructose1,6-bisphosphatase; FbPase). Quantitative RT-PCR revealed high levels both C- M-type PFK mRNA non-transgenic mouse cortex, whilst there was little L-type. In 24-month-old but not 7-, 13-, 17-month-old mice, copy number PFK-C significantly comparison littermates, while level other isoforms FbPase did differ between tissue samples. situ hybridization sections from aged plaque-associated neurons upregulation reactive astrocytes surrounding deposits. The decreased Western analysis accompanied enzyme comparisonto littermates. Our data impairment occurs only due long-lasting burden. This results reduction concomitant reactive, plaque-surrounding astrocytes.