Double mutant transgenic mice (
App/Ps1 mice) expressing a chimeric mouse/human amyloid precursor protein (
Mo/HuAPP695swe) and a mutant human presenilin 1 (
PS1-dE9) under the control of a prion protein promoter were purchased from the Jackson Laboratories. Breeding pairs of
Sirt3 knockout mice used to establish an in-house colony were a generous gift from David Gius (Northwestern University, Evanston, IL). Both mouse strains were on a congenic C57BL/6J background. Methods for genotyping have been described previously (datasheet on AppPs1 mouse strain 005864, Jackson Laboratories; and Cheng et al., 2016 (
link)).
Sirt3-haploinsufficient
App/Ps1 mice (
Sirt3±App/Ps1) were generated by cross-breeding Sirt3
± and AppPs1 mice as described previously (Cheng et al., 2020 (
link)). All animal procedures were approved by the Animal Care and Use Committee of the National Institute on Aging Intramural Research Program. Mice were provided a standard diet (Teklad
Global 18% Protein Rodent Diet, Envigo, Indianapolis, IN, USA). They were maintained on a 12 h light/dark cycle at 20–22 °C. All mice used in this study were male.
Perone I., Ghena N., Wang J., Mackey C., Wan R., Malla S., Gorospe M., Cheng A, & Mattson M.P. (2022). Mitochondrial SIRT3 Deficiency Results in Neuronal Network Hyperexcitability, Accelerates Age-Related Aβ Pathology, and Renders Neurons Vulnerable to Aβ Toxicity. Neuromolecular medicine, 25(1), 27-39.