B6129sf2 j

All animal experiments were conducted in accordance with the University of Virginia Institutional Animal Care and Use Committee. Animals were housed in a temperature and humidity controlled vivarium (22–24°C, ∼40% humidity) and were provided with food and water ad libitum. 3xTg experiments were conducted with 8–13 mo female 3xTg mice on a B6129 background (Oddo et al., 2003 (link)) (Jackson Laboratory #034830), with age-matched B6129SF2/J (Jackson Laboratory #101045) females as wild type controls. 5xFAD experiments were conducted with 7 mo female heterozygous 5xFAD mice on a C57BL/6J background (Oakley et al., 2006 (link)) (Jackson Laboratory #034848), with littermates genotyped as not expressing the mutant transgene serving as wild type controls. PS19 experiments were conducted with 7 mo female heterozygous PS19 mice on a B6C3 background (Yoshiyama et al., 2007 (link)) (Jackson Laboratory #008169), with littermates genotyped as not expressing the mutant transgene serving as wild type controls. For microglia depletion experiments, mice were given chow formulated with PLX3397 (660 mg/kg) or control chow for 7 days before light cycle shift and were maintained on PLX or control chow for the remainder of the experiment.

5xFAD wild-type (B6SJLF1/J; male n = 20, female n = 33) and transgenic (B6SJLTg(APPSwF1Lon,PSEN1*M146L*L286V)6799Vas/Mmjax; male n = 23, female n = 33) mice and 3xTG wild-type (B6129SF2/J; male n = 24, female n = 35) and transgenic (B6;129Psen1^tm1Mpm Tg(APPSwe, tauP301L)1Lfa/Mmjax; male n = 21, female n = 35) mice were obtained from Jackson Laboratory (Bar Harbor, USA). Because we were primarily comparing WT and TG mice, there was no random assignment to groups. A minimum of 7 mice per group were used for behavioural experiments; our previous work indicates power of 0.80 can be achieved with a sample size of 6 mice (α = 0.05). Differences in sample sizes between sexes was a result of attrition^{46 (link)}. Mice were housed in polyethylene cages (16 × 12 × 26 cm) with corncob bedding, crink-l’Nest and cotton nest squares and food (Tekland Global 16% Protein Rodent Maintenance Diet, Harlan Tekland, USA) and water available ad libitum. Mice were tested during the light phase of a 12 h light/dark cycle (0800 lights on; 2000h lights off). All procedures followed the guidelines of the Canadian Council on Animal Care and were approved by the Animal Care Committee at the University of Guelph and the University of Western Ontario (2006-103 and 2006-104). Object recognition testing started when mice were 12 months of age after they were tested in different touchscreen tasks.

Mice deficient in phagocyte NOX2 (NADPH oxidase, gp91^phox–/–; strain B6.129S-Cybbtm1Din/J; #002365) and age- and gender-matched control C57BL/6J (# 000664), or deficient in mitochondria superoxide dismutase 1 (SOD1) (strain B6;129S-Sod1tm1Leb/J, #002972) and age- and gender-matched B6129SF2/J control (#101045) were purchased from Jackson Laboratory (Bar Harbor, ME, USA). KO or control mice (n = 8/group) were infected by 10⁶P. berghei and evaluated for clinical scores and survival as described above. On day 6 p.i., an aliquot of blood was obtained to estimate parasitemia as above.

Male 3xTg-AD [B6129-Psen1tm1MpmTg (APPSwe, tauP30L) 1Lfa/J] [35 (link)] and wild-type mice (B6129SF2/J) were purchased from The Jackson Laboratory (Bar Harbor, ME, USA). The 3xTg-AD, overexpressing mutant amyloid precursor protein (APP (APPSwe)), presenilin 1 (PSEN1 (PS1M146V)), and hyperphosphorylated tau (tauP301L), were originally generated by co-injecting two independent transgene constructs encoding human APPSwe and tauP301L (4R/0 N) (controlled by murine Thy1.2 regulatory elements) into single-cell embryos harvested from mutant homozygous PS1M146V knock-in mice. Wild-type mice of mixed genetic background 129/C57BL6 were used as controls. These mice have been characterized and described by Oddo et al. [35 (link)]. The animals were maintained on a 12-h light/dark cycle in a temperature- and humidity-controlled rooms and food and water were available ad libitum.

Pathogen-free, male C57BL/6 mice, 6 to 8 weeks old, weighing 19 to 21 g were purchased from Orient Bio (Sungnam, Korea). B6.129-Mertk^tm1Gr1/J (MerTK^−/−) and wild-type (WT) control mice with an identical background (B6.129SF2/J) were obtained from The Jackson Laboratory (Bar Harbor, Maine, USA). STAT1^−/− mice were from the Charles River Laboratory. STAT1^−/− mice were on a C57BL/6 background (Orient Bio). MerTK^−/−, STAT1^−/−, and the respective WT mice were age-matched (7 to 10 weeks old) and sex-matched for all experiments. The Animal Care Committee of the Ewha Medical Research Institute approved the experimental protocol. Mice were cared for and handled in accordance with the National Institutes of Health (NIH) Guide for the Care and Use of Laboratory Animals.

Male 3xTg-AD mice [B6129-Psen1tm1MpmTg (APPSwe, tauP30L) 1Lfa/J] [25 (link)] and wild-type mice (B6129SF2/J) were purchased from Jackson Laboratories. The 3xTg-AD, overexpressing mutant APP (APPSwe), PSEN1 (PS1M146V), and hyperphosphorylated tau (tauP301L), were originally generated by co-injecting two independent transgene constructs encoding human APPSwe and tauP301L (4R/0 N) (controlled by murine Thy1.2 regulatory elements) in single-cell embryos harvested from mutant homozygous PS1M146V knock-in mice. Wild-type mice of mixed genetic background 129/C57BL6 were used as controls. These mice have been characterized and described by Oddo et al. [25 (link)]. The animals were maintained on a 12-h light/dark cycle in temperature- and humidity-controlled rooms, and food and water were available ad libitum. All experiments were carried out according to the Directive 2010/63/EU and the Italian law (D.Lgs. 26/2014), and were approved by the Italian Ministry of Health.