5xfad tg mice

Manufactured by Jackson ImmunoResearch

Sourced in Montenegro, United States

5XFAD Tg mice are a transgenic mouse model that overexpresses five familial Alzheimer's disease (AD) mutations. These mice display rapid, progressive amyloid-beta pathology and cognitive deficits, making them a useful tool for studying Alzheimer's disease.

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Lab products found in correlation

C57bl 6j female mice, by Daehan Biolink (1 mentions) C57bl 6j, by Jackson ImmunoResearch (1 mentions)

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5xFAD mice (70 citations) 5xFAD (41 citations) 5XFAD APP transgenic (TG) mice (2 citations)

4 protocols using 5xfad tg mice

Alzheimer's Pathology in 5XFAD Mice

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Three-month-old male 5XFAD Tg mice (n = 20) harboring both mutant human APP (K670N, M671L, I716V, V717I) and presenilin 1 (M146L * L286V), as well as their non-Tg control littermates (n = 16), were used in the present study. It has been reported that by age 3 months, Aβ plaques already start to appear in this mouse model (22 (link)); thus, we adopted this age to investigate the effects of CCH on Tg mice. 5XFAD Tg mice were purchased from Jackson Laboratories (Bar Harbor, ME) and maintained by crossing hemizygous Tg mice with non-Tg B6/SJL breeders (Jackson Laboratories). All newborn pups were screened for transgene expression by polymerase chain reaction analysis, as described in the Jackson Laboratory protocol. Mice were housed in groups of 2–4 per cage under standard laboratory conditions (12-hour light/dark cycle; lights on at 8:00–20:00, temperature: 23 ± 2 °C, and humidity: 50% ± 10%) with ad libitum access to food and water.

Kim M.S., Bang J., Kim B.Y, & Jeon W.K. (2021). Impaired Cognitive Flexibility Induced by Chronic Cerebral Hypoperfusion in the 5XFAD Transgenic Mouse Model of Mixed Dementia. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 76(7), 1169-1178.

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5xFAD Transgenic Mouse Model

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The 5xFAD Tg mice with a C57BL/6J genetic background were obtained from Jackson Laboratory (Bar Harbor, ME, USA) (strain: B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax; JAX MMRRC Stock #034848) [27 (link)]. These mice were bred with their congenic wild-type (WT) line, C57BL/6J female mice (Daehan Biolink, Eumseong, Republic of Korea). Following weaning, mice were co-housed with littermates under standard conditions (temperature, 20–25 °C; relative humidity, 45 ± 5%; light–dark cycle, 12 h:12 h) until the harvest dates. All mice had ad libitum access to a standard diet (Daehan BioLink, Eumseong, Republic of Korea). Male C57BL/6J WT mice were used as control animals.

Kim Y., Cho M., Jang C.H., Lee J.S., Kim J.S., Oh J, & Lim J. (2024). Oral Administration of Euonymus alatus Leaf Extract Ameliorates Alzheimer’s Disease Phenotypes in 5xFAD Transgenic Mice. Foods, 13(5), 682.

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Transgenic Mouse Model of Alzheimer's Disease

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All work with mice followed National Institutes of Health guidelines and was approved by the Stony Brook University Institutional Animal Care and Use Committee. Tg-5xFAD mice were obtained from Jackson Laboratories. Tg-5xFAD mice co-express human AβPP and human presenilin 1 with five familial AD mutations (AβPP K670N/M671L + I716V + V717I and PS1 M146L + L286V) and develop early-onset Aβ accumulation and fibrillar Aβ plaques in the brain starting at about two months of age (Oakley et al., 2006 (link)). Tg-MBP1-EGFP mice, generated as described below, were maintained as homozygous. The two transgenic lines were crossed for over two generations before the het/het mice used in this study were generated. Twenty mice of each group with equal numbers from both sexes were tested in behavioral measures prior to brain tissue collection.

Ou-Yang M.H., Xu F., Liao M.C., Davis J., Robinson J.K, & Van Nostrand W.E. (2014). The N-terminal region of myelin basic protein reduces fibrillar amyloid-β deposition in Tg-5xFAD mice. Neurobiology of aging, 36(2), 801-811.

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Characterization of Transgenic Alzheimer's Mice

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All work with mice followed National Institutes of Health guidelines and was approved by the Stony Brook University Institutional Animal Care and Use Committee (IACUC). Tg-SwDI mice were generated and characterized in our laboratory as previously described [27 (link)–29 (link)]. Tg-SwDI mice express the human Swedish/Dutch/Iowa AβPP transgene in neurons under control of the Thy1 promoter element and develop early-onset Aβ deposition and cerebral microvascular amyloid accumulation in the cortex, thalamus and subiculum. Tg-5xFAD mice were obtained from Jackson Laboratories. Tg-5xFAD mice express the human Swedish/Indiana mutant AβPP transgene in neurons also under control of the Thy1 promoter element and develop early-onset Aβ deposition and, in this case, parenchymal plaque amyloid accumulation in the cortex, thalamus and subiculum [30 (link)]. Six to eight heterozygous Tg-SwDI, heterozygous Tg-5xFAD, and wild-type mice were used for each 3 and 6 month timepoints.

Xu W., Xu F., Anderson M.E., Kotarba A.E., Davis J., Robinson J.K, & Van Nostrand W.E. (2014). Cerebral microvascular rather than parenchymal amyloid β-protein pathology promotes early cognitive impairment in transgenic mice. Journal of Alzheimer's disease : JAD, 38(3), 621-632.

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