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App ps1 mice

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The APP/PS1 mice are a genetically modified mouse model that expresses a mutant form of the amyloid precursor protein (APP) and presenilin 1 (PS1) genes. These mice develop Alzheimer's-like pathology, including the formation of amyloid-beta plaques in the brain. The APP/PS1 mice are used in research to study the mechanisms underlying Alzheimer's disease and to evaluate potential therapeutic interventions.

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Lab products found in correlation

C57bl 6j, by Jackson ImmunoResearch (4 mentions) App ps1, by Jackson ImmunoResearch (2 mentions) Fmr1 ko, by Jackson ImmunoResearch (2 mentions) Heparin, by Merck Group (1 mentions) Pv cre mice, by Jackson ImmunoResearch (1 mentions) Female wt mice, by Jackson ImmunoResearch (1 mentions) Sprague dawley, by Charles River Laboratories (1 mentions) C57bl 6 mice, by Jackson ImmunoResearch (1 mentions) C56bl 6j mice, by Jackson ImmunoResearch (1 mentions) Adult male sprague dawley rats, by BioLASCO (1 mentions) C57bl 6 mice, by BioLASCO (1 mentions) C57bl 6l mice, by Jackson ImmunoResearch (1 mentions) Km670 671nl, by Jackson ImmunoResearch (1 mentions) 5xfad mice, by Jackson ImmunoResearch (1 mentions) C57bl 6j mice, by Jackson ImmunoResearch (1 mentions) Wild type c57bl 6 mice, by Jackson ImmunoResearch (1 mentions) Appswe psen1de9 app ps1 mice, by Jackson ImmunoResearch (1 mentions)

Spelling variants of this product

APP/PS1 (28 citations) APP/PS1 double-transgenic mice (8 citations) APP/PS1 (APPswe + PSEN1dE9) transgenic mice (4 citations) Transgenic female APP-PS1 mice (4 citations) APP695/PS1-dE9 transgenic (APP/PS1) mice (3 citations) APPswe/PSEN1dE9 (APP/PS1) mice (3 citations) APP/PS1 transgenic mice (#34829-JAX) (2 citations) APPswe/PS1dE9 (APP/PS1) double transgenic mice (2 citations) APP/PS1 (Stock No. 004462) mice (2 citations) APP/PS1 mice stock 004462 (2 citations)

31 protocols using app ps1 mice

1

Transgenic AD Mouse Model Perfusion

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The same protocol was performed according to Muthukumaran et al. 2018. Experiments performed on animals were approved by the University of Windsor's Animal Care Committee in accordance with the Canadian Council of Animal Care guidelines. Twelve male double transgenic APP/PS-1 mice (Jackson Laboratory; strain: B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax) and six male C57BL/6 wild-type counterpart mice (Charles River Laboratories) were housed in groups of three or four. Transgenic mice were housed separately to avoid any social hierarchies due to functional neurological changes. The home cages contained baby-food jars, overturned cardboard cup holders, and cardboard tubes to provide environmental enrichment. Mice had continuous access to food and water, and their weight was measured once a week. The colony room was maintained at 20°C, and mice were under a controlled 12 hr : 12 hr dark-light cycle. Following the experimental period, the mice (approximately 18 months old) were euthanized and perfused using ice-cold PBS containing 28 μg/mL heparin (Sigma-Aldrich, Canada, Cat. No. H3393) followed by tissue fixation with ice-cold 10% formaldehyde made in PBS.
Vegh C., Pupulin S., Wear D., Culmone L., Huggard R., Ma D, & Pandey S. (2019). Resumption of Autophagy by Ubisol-Q10 in Presenilin-1 Mutated Fibroblasts and Transgenic AD Mice: Implications for Inhibition of Senescence and Neuroprotection. Oxidative Medicine and Cellular Longevity, 2019, 7404815.
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2

Transgenic Mouse Model for Alzheimer's

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Adult male Sprague-Dawley rats (250–300 g) and adult male APP/PS1 transgenic mice were used in this study. The APP/PS1 mice were purchased from Jackson Laboratory (Bar Harbor, ME, USA) (strain name: B6.Cg-Tg (APPswe,PSEN1dE9)85Dbo/Mmjax, stock number: 005864). They were all bred at the Animal Facility of the Institute of Biomedical Sciences (IBMS), Academia Sinica in Taiwan. All the animals were housed and maintained on a 12/12 h light/dark cycle (light on at 0630 hours) with food and water continuously available. Experimental procedures followed the Guidelines of Animal Use and Care of the National Institute of Health and were approved by the Animal Committee of IBMS, Academia Sinica.
Tao C.C., Hsu W.L., Ma Y.L., Cheng S.J, & Lee E.H. (2017). Epigenetic regulation of HDAC1 SUMOylation as an endogenous neuroprotection against Aβ toxicity in a mouse model of Alzheimer's disease. Cell Death and Differentiation, 24(4), 597-614.
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3

AZ59 Treatment in Alzheimer's Mice

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Mice were cared for by the Yale Animal Resource Center and all experiments were approved by Yale's Institutional Animal Care and Use Committee. Wild type and APP/PS1 mice were purchased from Jackson Laboratory and maintained on a C57/Bl6J background as described previously.8 Animals were randomly assigned to treatment groups and the experimenter was blinded to both genotype and treatment status. All mice utilized in the experiments received either control IgG or AZ59 diluted in PBS and weekly doses were administered by i.p. injection. The first cohort that received the 100 and 20 mg/kg doses of AZ59 began treatment at 12–13 months of age and was 64% female. The second cohort that received 20, 4, or 0.8 mg/kg AZ59 began treatment at 10–11 months of age and was 54% female. The mice used for biochemical signaling analysis began treatment at 13 months of age and was 44% female. Treatment continued throughout the course of all behavioral testing except where specified in the cohort 2 washout phase.
Cox T.O., Gunther E.C., Brody A.H., Chiasseu M.T., Stoner A., Smith L.M., Haas L.T., Hammersley J., Rees G., Dosanjh B., Groves M., Gardener M., Dobson C., Vaughan T., Chessell I., Billinton A, & Strittmatter S.M. (2019). Anti‐PrPC antibody rescues cognition and synapses in transgenic alzheimer mice. Annals of Clinical and Translational Neurology, 6(3), 554-574.
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4

Conditional Knockdown of Parvalbumin Neurons in APP/PS1 Mice

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APP/PS1 mice (The Jackson Laboratory; strain B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J; stock number 004462) express a chimeric mouse/human APP gene harboring the Swedish double mutation K595N/M596L (APPswe) and a human PS1 gene harboring the exon 9 deletion (PS1dE9), both under the control of the mouse prion protein promoter (MoPrP.Xho) [67 (link)–69 (link)]. PV-Cre mice (The Jackson Laboratory; strain B6.129P2-Pvalbtm1(cre)Arbr/J; stock number 017320) express Cre recombinase under the control of the mouse parvalbumin (Pvalb) promoter, directing Cre expression specifically to parvalbumin expressing cells [70 (link)]. All mouse lines were maintained on a C57BL/6 background. Hemizygous APP/PS1 mice were crossed with hemizygous PV-Cre mice to produce double-transgenic mice and single-transgenic controls. All experiments were performed with single-housed male mice and approved by the Central Committee for Animal Experiments (CCD) and the Animal Welfare Body (IVD) of the VU University Amsterdam.
Hijazi S., Heistek T.S., Scheltens P., Neumann U., Shimshek D.R., Mansvelder H.D., Smit A.B, & van Kesteren R.E. (2019). Early restoration of parvalbumin interneuron activity prevents memory loss and network hyperexcitability in a mouse model of Alzheimer’s disease. Molecular Psychiatry, 25(12), 3380-3398.
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5

Alzheimer's Disease Mouse Model Protocol

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One-month-old female APP/PS1 mice (Mutant Mouse Resource and Research Center 34832) and age-matched female WT mice were purchased from Jackson Laboratory. The transgenic mouse is generated on a genetic background C57BL/6J expressing Swedish mutation KM670/671NL of human APP (APPswe) and a presenilin 1 lacking exon 9 (PSEN1dE9) (27 (link)). After 6 to 8 weeks, the transgenic mice showed cerebral amyloidosis and amyloid-associated pathologies, including dystrophic synaptic buttons, robust gliosis, and increase in microglia number and activation (29 (link)). All protocols for animal use here were approved by the Institutional Animal Care and Use Committee. Animals were treated in accordance with good animal practice following National Institutes of Health requirements.
He P., Schulz P, & Sierks M.R. (2021). A conformation-specific antibody against oligomeric β-amyloid restores neuronal integrity in a mouse model of Alzheimer's disease. The Journal of Biological Chemistry, 296, 100241.
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6

Longitudinal Study of APP/PS1 Mice

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APPswe/PS1dE9 C57BL/6 J double-transgenic (APP/PS1) mice at different ages ranging from 1-month to 6-month old and age-match wild type (WT) mice were used in the present study. Male heterozygous APP/PS1 mice were obtained from Jackson Laboratory (Bar Harbor, ME, USA) and used to mate with female C57BL/6 mice to generate heterozygous mice and WT littermates for this research. The genotypes of APP/PS1 animals were identified by standard polymerase chain reaction (PCR) analysis of genomic DNA isolated from mouse tails. All mice were housed in groups and accessed to food and water ad libitum in a 12:12 h light–dark (light on at 8: 00 am) cycle, provided with controlled temperature and humidity.
Xie Y., Yan L., Zeng H., Chen W., Lu J.H., Wan J.B., Su H, & Yao X. (2020). Fish oil protects the blood–brain barrier integrity in a mouse model of Alzheimer’s disease. Chinese Medicine, 15, 29.
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7

Aged APP/PS1 Mouse Model for Alzheimer's Research

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In the present study, the double transgenic APPswe/PS1ΔE9 (APP/PS1) AD mouse model, introduced by Jankowsky et al. in 2004 [32 (link)], was used, its pathology and behavioral deficits having been well characterized. At 6 months of age, the mice develop Aβ deposits, gliosis, and cognitive deficits, which are especially detectable in the Morris water maze (MWM). The pathology and cognitive deficits progressively intensify with age [32 (link)–35 (link)]. APP/PS1 mice were ordered from the Jackson Laboratory (Jackson Laboratory, USA) and bred in-house, in a controlled environment, on a light/dark cycle (12/12 h), with 54% humidity and a temperature of 22 °C. Food and water were available ad libitum. All experiments were performed in accordance with the German Law on the protection of animals (TierSchG §§ 7–9) and were approved by a local ethics committee (LANUV, North-Rhine-Westphalia, Germany, reference number: 84-02.04.2011.A359).
Aged male APP/PS1 mice (n = 21) and their non-transgenic littermates (n = 11) were tested in the present study (average age at treatment initiation: 18 months ± 3 weeks). During the study, all mice were housed single caged.
Schemmert S., Schartmann E., Zafiu C., Kass B., Hartwig S., Lehr S., Bannach O., Langen K.J., Shah N.J., Kutzsche J., Willuweit A, & Willbold D. (2018). Aβ Oligomer Elimination Restores Cognition in Transgenic Alzheimer’s Mice with Full-blown Pathology. Molecular Neurobiology, 56(3), 2211-2223.
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8

Bilobalide Treatment in APP/PS1 Mice

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Our study was approved by the Institutional Ethics Committee of Zhongshan Hospital, Fudan University. All animal experiments were performed in accordance with the Institutional Animal Care and Use Committee. APP/PS1 mice were from Jackson laboratory (#004462). Male APP/PS1 mice (12 month old) were intraperitoneally injected with bilobalide (n = 6, 0.5 mg/kg) or DMSO control (n = 6) every week for 4 weeks.
Xiang J., Yang F., Zhu W., Cai M., Li X.T., Zhang J.S., Yu Z.H., Zhang W, & Cai D.F. (2021). Bilobalide inhibits inflammation and promotes the expression of Aβ degrading enzymes in astrocytes to rescue neuronal deficiency in AD models. Translational Psychiatry, 11, 542.
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9

40-Hz Light Flicker in APP/PS1 Mice

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Adult (female, age 8 months) APP/PS1 mice were obtained from the Jackson Laboratory, with their non-transgenic wild-type (WT) littermates as control. Female WT mice were divided randomly into two groups (n = 10 per group): A control group (control) and a 40-Hz light flicker group (40 Hz). APP/PS1 mice were divided randomly into two groups (n = 10 per group): An APP/PS1 group (APP/PS1) and an APP/PS1 plus 40-Hz light flicker group (APP/PS1 + 40 Hz). Mice were housed under a 12-h light/12-h dark cycle (temperature ∼25°C; humidity ∼40%). The experiment procedures were approved by the Institutional Animal Care and Use Committee of Shenzhen University (resolution number, 2017003). All efforts were made to reduce animal suffering.
Yao Y., Ying Y., Deng Q., Zhang W., Zhu H., Lin Z., Zhang S., Ma J, & Zhao Y. (2020). Non-invasive 40-Hz Light Flicker Ameliorates Alzheimer’s-Associated Rhythm Disorder via Regulating Central Circadian Clock in Mice. Frontiers in Physiology, 11, 294.
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10

Transgenic Alzheimer's Mouse Models

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All animal procedures were approved by the Animal Care and Use Committee of Cleveland Clinic. Adult male Sprague–Dawley (250–300 g, 2–3 mo of age, Charles River) rats were used, and all experiments were performed during the light cycle. Tg-APPsw/PSEN1DE9 (APP/PS1, MMRRC Stock No: 41848-JAX), and C57BL/6 mice were purchased from Jackson Laboratory, regularly maintained and studied at six months old. Tg-APPsw/PSEN1DE9 mice were obtained as hemizygote by crossing the transgenics with animals on a C57BL/6 background. During experiment, non-transgenic littermates were used as the control for the transgenic mice with the same age (6 months old) and gender ratio (male/female ratio about 1). Metabotropic glutamate receptor 1 mutant mice (Grm1−/−, C57BL/6J-Grm1rcw−3J/GrsrJ, Jackson Laboratory stock No. 005521) crossed with APP/PS1 mice to generate the new strain (APP/PS1/Grm1−/−), which was validated by genotyping following the protocols provided by Jackson Laboratory. Experiments were conducted in mice at the age of 6 mo. The animals were randomly assigned to different groups with specific treatment, and another party blinded the experimenter to the individual groups. No statistical methods were used to predetermine sample sizes, but our sample sizes are similar to those reported in previous publications [30 (link),3 (link)].
Bie B., Wu J., Foss J.F, & Naguib M. (2019). Activation of mGluR1 mediates C1q-dependent microglial phagocytosis of glutamatergic synapses in Alzheimer’s rodent models. Molecular neurobiology, 56(8), 5568-5585.
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