Early metabolic changes in the brain of Alzheimer's disease rats are driven by GLAST+ cells.

ABSTRACT: Glucose metabolic dysfunction is a hallmark of Alzheimer's disease (AD) pathology and is used to diagnose the disease or predict imminent cognitive decline. The main method to measure brain metabolism in vivo is positron emission tomography with 2-Deoxy-2-[¹⁸F]fluoroglucose ([¹⁸F]FDG-PET). The cellular origin of changes in the [¹⁸F]FDG-PET signal in AD is controversial. We addressed this by combining [¹⁸F]FDG-PET with subsequent cell-sorting and γ-counting of [¹⁸F]FDG-accumulation in sorted cell populations. 7-month-old male TgF344-AD rats and wild-type controls (n = 24/group) received sham or ceftriaxone (200 mg/kg) injection prior to [¹⁸F]FDG-PET imaging to increase glutamate uptake and glucose utilisation. The same

SUBMITTER: Morrey WJ 

PROVIDER: S-EPMC11806453 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature