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Appswe psen1de9

Manufactured by Jackson ImmunoResearch
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The APPswe/PSEN1dE9 is a transgenic mouse model that expresses both the human amyloid precursor protein (APP) with the Swedish (K670N/M671L) mutation and the human presenilin 1 (PSEN1) with the dE9 deletion. This model is commonly used in Alzheimer's disease research to study the pathogenesis and progression of the disease.

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11 protocols using appswe psen1de9

1

Transgenic Mouse Model of Alzheimer's

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AβPP/PS1 (APPswe, PSEN1dE9) double transgenic mice were originally purchased from Jackson Laboratory and have been maintained on a C57BL/6 background. The AβPP/PS1 (B6.CgTg (AβPPswe, PSEN1dE9) 85Dbo/Mmjax) transgenic animals express human AβPP with a mutation that in humans causes familial AD and the amyloid beta (A4) precursor protein (Mo/HuAPP695swe). In addition they express and the human PSEN1 with a mutation that in humans also causes familial AD due to presenilin 1(PS1-dE9). Five male AβPP/PS1 mice and their C57BL/6 (wild type) littermate controls were provided food and water ad libitum and housed in a 12-h light/dark cycle until 13 months of age, then euthanized via CO2 asphyxiation followed by cervical dislocation and cardiac exsanguination. The investigation conforms to the Guide for the Care and Use of Laboratory Animals (eighth edition, 2010). Animal use was approved by the University of North Dakota IACUC.
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2

Transgenic Mouse Model of Alzheimer's Disease

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All experimental procedures and methods involving animals were approved by Dankook University Animal Care and Use Committee (1D: 13-033). All mice used in this study were housed in individual cages under temperature- and light-controlled (12 h light/12 h dark cycle) specific pathogen-free conditions. They were allowed free access to standard irradiated chow (Purina Mills, Seoul, Republic of Korea) and water.
AD model Tg mice (APPswe/PSEN1dE9) were purchased from Jackson Laboratory (Bar Harbor, ME, USA). These mice express chimeric mouse/human amyloid precursor protein (Mo/HuAPP695swedish) and mutant human presenilin 1 (PSEN1 deletion exon 9). The humanized Mo/HuAPP695swe transgene allows the mice to secrete a human A-beta peptide. They were maintained as double-hemizygotes by crossing with C57BL6 wild-type mice. For genotyping, genomic DNA was extracted from mice tails using an EzDirectTM Mouse Direct PCR kit (Wizbiosolutions Inc., Gyeonggi-do, Republic of Korea) according to the protocol provided by the company. Positive-Tg genotype was detected by polymerase chain reaction (PCR) analysis using the following primers: human PS1-forward, 5′-AAT AGA GAA CGG CAG GAG CA-3′; and human PS1-reverse, 5′-GCC ATG AGG GCA CTA ATC AT-3′.
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3

Transgenic Mouse Model for Alzheimer's

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Female APPswe/PSEN1dE9 (henceforward APP/PS1) transgenic mice with 5–9 months were initially purchased from The Jackson Laboratory (MMRRC stock #34832; donated by Dr. David R Borchelt, University of Florida). To maintain the colonies, male hemizygous APP/PS1 mice were crossed with female WT mice. In this study, 8–9 months old mice were obtained by crossing female WT (B6C3F1/J) mice with male hemizygous APP/PS1 mice. All mice were kept in cages with 1–3 littermates and with ad libitum food and water. The cages were kept at 21–23 °C with 50–60% humidity under a 12 h dark/light cycle with light from 7AM to 7PM. All procedures were carried out in accordance with the guidelines of the European Community guidelines (EU Directive 2010/63/EU) and the Portuguese law on animal care (1005/92) and approved by the Ethical Committee of the Center for Neuroscience and Cell Biology of (ORBEA n° 243_2020/1210-72020).
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4

Transgenic Mouse Models for Alzheimer's

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Tg2576 mice (C57/Bl6;SJL background, stock no. 001349) carrying the human APP (APP695) gene containing the double Swedish mutations (K670N and M671L) under the control of the hamster prion promoter were obtained from Taconic Europe. APPswe/PSEN1dE9 (also known as APP/PS1, stock no. 034829) carrying a chimeric mouse/human APP695 and a mutant human presenilin 1 (PSEN1dE9) were obtained from The Jackson Laboratory. Wild-type C57/Bl6J mice were sourced from The Jackson Laboratory and bred on-site in the Smurfit Institute of Genetics in Trinity College Dublin (TCD).
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5

Alzheimer's Disease Mouse Model with SVCT2

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Heterozygous SVCT2 knockout mice (SVCT2+/−; Sotiriou et al., 2002 (link)) were crossed with a bigenic mouse carrying two mutations known to cause familial (early-onset) AD (APPSWE/PSEN1dE9; Jackson Laboratories, stock #005864; Fig. 1A). Mice aged 12 to 18 weeks, were maintained in a temperature and humidity controlled environment with ad libitum access to food and water. These mice can synthesize ASC and received no additional supplementation. All procedures were approved by the Institutional Animal Care and Use Committee and were conducted in accordance with the NIH Guide for the Care and Use of Laboratory Animals. All experiments were run, and data analyzed, with the experimenter blinded to genotype.
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6

Alzheimer's Mouse Model Virus Injection

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All animal experiments were performed on a mouse model for AD carrying mutations APPswe/PSEN1dE9 (APP/PS1 mice of B6C3 hybrid background) to mimic amyloidosis (RRID: MMRRC_034829-JAX) originated from Jackson Laboratory (USA, stock number 004462). Mouse genotype was verified by performing PCR using the following primers: APP/PS1_F-5′ AAT AGA GAA CGG CAG GAG CA 3′; APP/PS1_R-5′ GCC ATG AGG GCA CTA ATC AT 3′. 10–12 month old animals of both sexes were used for the virus injection experiment, transgenic mice matched with WT littermates. Animals were maintained in a 12:12 light dark cycle (lights out at 20:00) and provided with food pellets and water ad libitum. Care and handling of animals were in accordance with the guidelines of the Institutional Animal Care and Use Committee of IBS (Daejeon, South Korea).
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7

Transgenic Alzheimer's Mouse Model

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All procedures were approved by the Rockefeller University Institutional Animal Care and Use Committee. All mice were housed with a 12-hour light/12-hour dark cycle and fed ad libitum. Transgenic mouse lines (2xTg: APPswe/PSEN1dE9; 1xTg: Tg2576 harboring HuAPP695.KM670/671NL; 3xTg: PS1M146V, APPswe and tauP301L], and C57BL/6J WT mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA). Mice were anesthetized via Nembutal IP injection (50-100 µl) and intracardiac perfusion was performed first with 20 ml ice cold PBS then 20 ml ice cold PBS with 4% paraformaldehyde. Dissected cerebral tissue was post-fixed overnight in PBS with 4% PFA at 4°C followed by 1 hour at room temperature.
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8

Aging and Alzheimer's in APP/PS1 Mice

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Male wild type (WT) and APP/PS1 (APPswe, PSEN1dE9 from Jackson Laboratory, Sacramento, CA, USA) mice (11.5–12-month-old, 20–25 g/each mouse) with a genetic background of C57BL/6J were used. The mice were reared with strict specific-pathogen-free (SPF) conditions (room temperature at 25 °C and 12 h light-dark cycle), and had free access to standard rodent water and food. Experiments were performed under a project license (No.: 2021-AE026) granted by the Institutional Animal Care Committee of Hebei Medical University, in compliance with AAALAC and the IACUC guidelines for the care and use of animals.
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9

Transgenic Mouse Models for Alzheimer's

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Tg2576 mice (C57/Bl6;SJL background, stock no. 001349) carrying the human APP (APP695) gene containing the double Swedish mutations (K670N and M671L) under the control of the hamster prion promoter were obtained from Taconic Europe. APPswe/PSEN1dE9 (also known as APP/PS1, stock no. 034829) carrying a chimeric mouse/human APP695 and a mutant human presenilin 1 (PSEN1dE9) were obtained from The Jackson Laboratory. Wild-type C57/Bl6J mice were sourced from The Jackson Laboratory and bred on-site in the Smurfit Institute of Genetics in Trinity College Dublin (TCD).
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10

Kenpaullone Alleviates AD Pathology

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APP/PS1 mice carrying Swedish APP and Presenilin one delta exon nine mutations (APPswe, PSEN1dE9) were purchased from the Jackson laboratory and bred in the Experimental Animal Center of Chongqing Medical University. All the experimental protocols were approved by the Ethics Committee of Chongqing Medical University following international standards. To assess the effect of kenpaullone (KEN) alone, APP/PS1 or wild‐type mice (12‐month‐old, female) with the same background identified by genotyping were i.p. injected with KEN (7 mg k−1g, every other day) for 2 months. For SHMT2 shRNA combined with KEN experiments, APP/PS1 mice (6‐month‐old, male) were randomly divided into three groups: bilateral hippocampus injection of adeno‐associated virus bearing control RNA, and SHMT2 shRNA without and with KEN (7 mg k−1g, every other day) for 2 months.
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