The 3×Tg-AD mice (Stock Number: 034830-JAX, RRID: MMRRC_034830-JAX) with APP, PS1, and tau mutations and non-transgenic B6129SF2/J wild-type (WT) mice (Stock Number: 101045, RRID: IMSR_JAX:101045) were obtained from The Jackson Laboratory (Bar Harbor, ME, USA). The 3×Tg-AD and WT mice were coordinated to reproduce at the same time. Gene identification was performed at 1 month of age, and the 3-month-old male offspring, which were selected to avoid estrogen interference on learning and memory function (Xing et al., 2013), were used in the experimental study. All mice were maintained in a specific pathogen-free animal room with food and water ad libitum and a 12-hour light/dark cycle. The experimental procedures in this study are shown in Figure 1
Tg ad mice
Manufactured by Jackson ImmunoResearch
Sourced in United States
The 3xTg-AD mice are a transgenic mouse model that expresses three mutant human genes associated with Alzheimer's disease: amyloid precursor protein (APP), presenilin 1 (PSEN1), and tau. These mice exhibit progressive cognitive deficits and neuropathological features similar to those observed in Alzheimer's disease patients.
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Lab products found in correlation
Semet, by Merck Group (2 mentions)
Pen strep, by Thermo Fisher Scientific (2 mentions)
Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (2 mentions)
Fetal bovine serum (fbs), by Thermo Fisher Scientific (2 mentions)
Non transgenic b6129sf2 j wild type mice, by Jackson ImmunoResearch (1 mentions)
Ps1m146v, by Jackson ImmunoResearch (1 mentions)
14 protocols using tg ad mice
1
3xTg-AD Mouse Model of Alzheimer's
2
Selenium Supplementation in 3xTg-AD Mice
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3×Tg-AD mice (4 months old), purchased from the Jackson Laboratory (Bar Harbor, Maine, ME, USA), were kept with accessible food and water under a 12-h light/dark cycle [69 (link)]. All animal experiments and procedures were approved by the Ethics Committee of Shenzhen University (Permit Number: AEWC-20140615-002, 15 July 2014). Mice (n = 6; 6 males and 6 females) were treated with 6 μg/mL Se-Met (Sigma-Aldrich, Santa Clara, CA, USA) in drinking water or received normal drinking water for 3 months.
3
In vitro and in vivo models of Alzheimer's disease
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HT22 cells, BV2 cells and bEnd.3 cells were cultured in DMEM (Gibco, USA) containing 10% FBS (Gibco, Australia), 1% Pen-Strep (100X, Gibco, USA) and 1% Non-Essential Amino Acids (100X, Gibco, USA) at 37 °C in a humidified 5% CO2 incubator.
Triple-transgenic AD (3 × Tg-AD) mice (B6; 129-Tg (APPSwe, tauP301L)1Lfa Psen 1tm1Mpm/Mmjax, male and female in half) were obtained from the Jackson Laboratory (Bar Harbor, ME, USA). Age- and gender-matched wild-type (WT) mice were purchased from Shanghai Model Organisms Center (Shanghai, China). All mice were bred in specific pathogen-free conditions with 12 h light/dark circles, constant temperature at 23 ± 1 °C, and relative humidity at 55 ± 5%. All experimental procedures were executed according to the protocols approved by Institutional Animal Care and Use Committee (IACUC), School of Pharmacy, Fudan University (No. 2020-04-YJ-ZQZ-01).
Triple-transgenic AD (3 × Tg-AD) mice (B6; 129-Tg (APPSwe, tauP301L)1Lfa Psen 1tm1Mpm/Mmjax, male and female in half) were obtained from the Jackson Laboratory (Bar Harbor, ME, USA). Age- and gender-matched wild-type (WT) mice were purchased from Shanghai Model Organisms Center (Shanghai, China). All mice were bred in specific pathogen-free conditions with 12 h light/dark circles, constant temperature at 23 ± 1 °C, and relative humidity at 55 ± 5%. All experimental procedures were executed according to the protocols approved by Institutional Animal Care and Use Committee (IACUC), School of Pharmacy, Fudan University (No. 2020-04-YJ-ZQZ-01).
4
Tg-AD Mouse Model for Neurodegeneration
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3 × Tg-AD mice, expressing human gene mutants
APPswe, PS1M146V, and tauP301L and wild-type (WT) mice of same genetic
background, were purchased from the Jackson laboratory (BarHarbor,
ME) for breeding. Male and female mice were kept in a separated cage
with ad libitum food and water supply with 12 h light/dark cycle prior
to treatment.
APPswe, PS1M146V, and tauP301L and wild-type (WT) mice of same genetic
background, were purchased from the Jackson laboratory (BarHarbor,
ME) for breeding. Male and female mice were kept in a separated cage
with ad libitum food and water supply with 12 h light/dark cycle prior
to treatment.
5
Hydrogen-Rich Water Mitigates Alzheimer's Pathology
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The HRW was gifted from Beijing Vitality Hydrogen Source Beverage Ltd. (Beijing, China), and the hydrogen concentration was greater than 1.6 parts per million. The triple transgenic (3×Tg)-AD model mice expressed the mutant human genes TauP301L and APPswe, and the mutant mouse gene PS1M146V. According to previous research on this mouse model (Oddo et al., 2003; Billings et al., 2005), Aβ begins to accumulate in the neurons at 4 months old, and gradually spreads outside the neurons. The accumulation of Aβ may cause neuronal dysfunction, which can lead to cognitive deficits. The 3×Tg-AD mice (n = 30, 25–30 g) and B6:129SF2/J (wild-type, WT) mice (n = 15, 25–30 g) were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). To avoid the influences of sex and estrogen, three-month-old male mice only were used in the study. The 3×Tg-AD mice were randomly divided into 3×Tg-AD (AD; n = 15) and HRW-treated 3×Tg-AD (AD + HRW; n = 15) groups, and the B6:129SF2/J mice were used as controls (n = 15). After being trained with a time-limited water supply (water was only provided from 10:00 a.m. to 2:00 p.m. every day) for 30 days, the 3-month-old 3×Tg-AD mice in the AD + HRW group were given HRW for 7 months, while the mice in the AD group were treated with normal drinking water for 7 months.
6
In vitro and in vivo models of Alzheimer's disease
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HT22 cells, BV2 cells and bEnd.3 cells were cultured in DMEM (Gibco, USA) containing 10% FBS (Gibco, Australia), 1% Pen-Strep (100X, Gibco, USA) and 1% Non-Essential Amino Acids (100X, Gibco, USA) at 37 °C in a humidified 5% CO2 incubator.
Triple-transgenic AD (3 × Tg-AD) mice (B6; 129-Tg (APPSwe, tauP301L)1Lfa Psen 1tm1Mpm/Mmjax, male and female in half) were obtained from the Jackson Laboratory (Bar Harbor, ME, USA). Age- and gender-matched wild-type (WT) mice were purchased from Shanghai Model Organisms Center (Shanghai, China). All mice were bred in specific pathogen-free conditions with 12 h light/dark circles, constant temperature at 23 ± 1 °C, and relative humidity at 55 ± 5%. All experimental procedures were executed according to the protocols approved by Institutional Animal Care and Use Committee (IACUC), School of Pharmacy, Fudan University (No. 2020-04-YJ-ZQZ-01).
Triple-transgenic AD (3 × Tg-AD) mice (B6; 129-Tg (APPSwe, tauP301L)1Lfa Psen 1tm1Mpm/Mmjax, male and female in half) were obtained from the Jackson Laboratory (Bar Harbor, ME, USA). Age- and gender-matched wild-type (WT) mice were purchased from Shanghai Model Organisms Center (Shanghai, China). All mice were bred in specific pathogen-free conditions with 12 h light/dark circles, constant temperature at 23 ± 1 °C, and relative humidity at 55 ± 5%. All experimental procedures were executed according to the protocols approved by Institutional Animal Care and Use Committee (IACUC), School of Pharmacy, Fudan University (No. 2020-04-YJ-ZQZ-01).
7
Effects of Rosmarinic Acid on 3xTg-AD Mice
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Six to eight-week-old male 3 × Tg-AD mice (The Jackson Laboratory, ME, USA), which express amyloid precursor protein Swe, tauP301L, and presenilin 1M146V, were divided into two groups: control group (n = 8) on a normal AIN-93G diet prepared in our laboratory from essential ingredients (Oriental Yeast, Shiga, Japan) and RA group (n = 9) on a normal diet supplemented with 0.5% RA. Mice were housed under controlled conditions with a temperature of 20–26 °C and a humidity of 40–60% under a 12/12-h light-dark cycle, with ad libitum food and water intake. Body weight and food consumption were measured twice weekly. After 8 months, all mice were sacrificed under isoflurane anesthesia and blood and organs were collected. The study was approved by the animal experiment committee of the University of Tokyo and performed in accordance with relevant guidelines and regulations (approval number, P16-224).
8
Selenium-Methionine Supplementation in 3xTg-AD Mice
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3× Tg-AD mice (4-month-old), purchased from the Jackson Laboratory (Bar Harbor, Maine, ME, USA), were kept with accessible food and water under a 12-h light/dark cycle [48 (link),49 (link)]. All animal experiments and procedures were approved by the Ethics Committee of Shenzhen University (Permit Number: AEWC-20140615-002). Mice (n = 24; 12 males and 12 females) were respectively treated with 6 µg/mL Se-Met (Sigma-Aldrich, Santa Clara, CA, USA) in drinking water or normal drinking water for 12 weeks and the body weight of each mouse was recorded every two weeks.
9
Alzheimer's Disease Model in Mice
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Male Triple-transgenic Alzheimer’s disease (3 × Tg-AD) and C57BL/6J were used in the present study. 3 × Tg-AD mice (harboring PS1M146V knockin, APPswe, and TauP301L transgenes) were acquired from The Jackson Laboratory. Age and sex matched C57BL/6J mice were employed as non-transgenic (non-Tg) controls. The study was performed on 3-month-old 3 × Tg-AD (n = 72) and non-Tg mice (n = 60). All animals were given ad libitum access to food and water in a room maintained at controlled temperature (23 ± 1 °C) and humidity (40–60%), with a 12 h light-dark cycle. All animal maintenance and use were in accordance with protocols approved by the ethical committee of Beijing Sport University (2015015).
10
Transgenic 3xTg AD Mouse Model
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The 3 × Tg AD mice (Jackson Laboratory, Sacramento, CA, USA) were housed under a 12-h light/dark cycle with access to food and water at 25 °C. All animal studies were approved by the Ethics Committee of Tongji Medical College, Huazhong University of Science and Technology. The information for primary antibodies employed in the current study is listed in Additional file 1 : Table S1.
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