Overview

Also Known As: 5XFAD

5XFAD transgenic mice overexpress both mutant human APP(695) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations and human PS1 harboring two FAD mutations, M146L and L286V. Expression of both transgenes is regulated by neural-specific elements of the mouse Thy1 promoter to drive overexpression in the brain. These 5XFAD transgenic mice rapidly recapitulate major features of Alzheimer's Disease amyloid pathology and may be useful models of intraneuronal Aβ-42 induced neurodegeneration and amyloid plaque formation.

Donating Investigator

IMR Colony, The Jackson Laboratory

Genetic overview

Genetic Background	Generation
	N6+N3 (2019-12-06 00:00:00)

Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Allele Type
Transgenic (Inserted expressed sequence, Humanized sequence)

View Genetics

Research Applications

Neurobiology Research
Research Tools
Mouse/Human Gene Homologs

View All Research Applications

Details

Detailed Description

Hemizygous mice are viable and fertile. These 5XFAD transgenic mice overexpress both mutant human APP(695) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations and human PS1 harboring two FAD mutations, M146L and L286V. Expression of both transgenes is regulated by neural-specific elements of the mouse Thy1 promoter to drive overexpression in the brain. Mice from this founder line have high APP expression correlating with high burden and accelerated accumulation of the 42 amino acid species of beta-amyloid (Aβ-42). 5XFAD mice generate Aβ-42 almost exclusively and rapidly accumulate massive cerebral levels. On the mixed C57BL/6 and SJL background background (see MMRRC stock 34840), intraneuronal Abeta;-42 accumulation is observed starting at 1.5 months of age, just prior to amyloid deposition and gliosis, which begins at two months of age. On a congenic C57BL/6J genetic background (see MMRRC stock 34848) it has been the observation of the MMRRC that this phenotype is not as robust as that demonstrated in the mixed C57BL/6 and SJL background (view data). In addition, these mice have reduced synaptic marker protein levels, increased p25 levels, neuron loss, and memory impairment in the Y-maze test. 5XFAD transgenic mice rapidly recapitulate major features of Alzheimer's Disease amyloid pathology and may be useful models of intraneuronal Aβ-42 induced neurodegeneration and amyloid plaque formation.

This strain does not carry the retinal degeneration allele Pde6b^rd1.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development

A transgene was designed with a mutant human amyloid beta (A4) precursor protein (APP) cDNA sequence (altered to include the APP K670N/M671L (Swedish) + I716V (Florida) + V717I (London) Familial Alzheimer's Disease (FAD) mutations) inserted into exon 2 of the mouse Thy1 gene. A second transgene was designed with a mutant human presenilin 1 (Alzheimer disease 3) (PSEN1 or PS1) cDNA sequence (altered to include the PS1 M146L + L286V FAD mutations) inserted into exon 2 of the mouse Thy1 gene. Both transgenes were added together in equal proportions and co-injected into the pronuclei of single-cell "C57/B6XSJL" hybrid embryos. Founders from the highest APP expressing line (Tg6799) were bred with (B6/SJL)F1 for more than 10 generations with stable germ-line transmission and expression of both transgenes, demonstrating that these "5XFAD" mice breed as single transgenics. The mice were then backcrossed to C57BL/6J mice using a speed congenic protocol and the retinal degeneration allele Pde6b^rd1 was bred out of the strain. Of note, the APP transgene includes the 5' untranslated region and thus contains a putative interleukin-1beta translational enhancer element.

Expression Data

Expressed Gene	PSEN1, presenilin 1, human
Expressed Gene	APP695, amyloid beta (A4) precursor protein (chimeric), mouse/human chimera
Site of Expression

Control Suggestions

Noncarrier
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Oakley H; Cole SL; Logan S; Maus E; Shao P; Craft J; Guillozet-Bongaarts A; Ohno M; Disterhoft J; Van Eldik L; Berry R; Vassar R. 2006. Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. J Neurosci 26(40):10129-40PubMed: 17021169 MGI: J:112949

View All References

Genetics

Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Allele Symbol: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Allele Name	transgene insertion 6799, Robert Vassar
Allele Type	Transgenic (Inserted expressed sequence, Humanized sequence)
Allele Synonym(s)	Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas; transgene insertion 6799, Robert Vassar
Gene Symbol and Name	Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas, transgene insertion 6799, Robert Vassar
Gene Synonym(s)	5XFAD line Tg6799; 5XFAD; Tg6799
Promoter	Thy1, thymus cell antigen 1, theta, mouse, laboratory
Expressed Gene	PSEN1, presenilin 1, human
Expressed Gene	APP695, amyloid beta (A4) precursor protein (chimeric), mouse/human chimera
Strain of Origin	(C57BL/6 x SJL)F1
Chromosome	3
General Note	Three transgenic lines coexpressing the APP and PSEN1 proteins at high, medium and low levels, respectively designated Tg6799, Tg7031, and Tg7092, were propagated for analysis, most of which employed Tg6799. Phenotypic Similarity to Human Syndrome: Macular Degeneration, Age-Related J:214858.
Molecular Note	Four familial Alzheimer disease- (FAD-) associated mutations were introduced into a single human amyloid precursor protein cDNA: the "Swedish" double mutation (K670N/M671L); the "Florida" mutation (I716V); and the "London" mutation (V717I). Two FAD-associated mutations, M146L and L286V, likewise were introduced into a human presenilin 1 cDNA. Each cDNA was then cloned independently into the mouse thymus cell antigen 1 gene, replacing a segment that contains thymus-specific elements so that expression of the transgenes is targeted only to the brain. Equal molar amounts of the two transgenes were coinjected into pronuclei of single-celled embryos.
Mutations Made By	Robert Vassar, Northwestern University

Disease/Phenotype

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Neurobiology Research
- Alzheimer's Disease
  - APP and PSEN1 mutants
  - Presenilin mutants
  - strains expressing mutant APP
- Neurodegeneration
Research Tools
- Neurobiology Research
Mouse/Human Gene Homologs
- Alzheimer's

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
involves: C57BL/6 * SJL

behavior/neurological phenotype

abnormal spatial learning
- by 4-5 months of age, defects in Y-maze alternation are detected in transgenic mice, indicating impaired spatial learning/memory

homeostasis/metabolism phenotype

amyloid beta deposits
- amyloid deposition increases rapidly with increasing age
- mice show Abeta₄₂ deposits at 2 months of age; Abeta₄₀ levels are lower in amyloid deposits; mice show robust intraneuronal amyloid deposition
- plaques appear first in deep cortical layers and in subiculum, and spread with age to fill most of cortex, subiculum and hippocampus; also, less numerous deposits are observed in thalamus, brainstem and olfactory bulb in older mice

immune system phenotype

brain inflammation
- transgenic mice display neuroinflammation

nervous system phenotype

abnormal hippocampus morphology
- cortical layer 1 is significantly thinner than in control brains

abnormal neuron morphology
- some neurons contain intraneuronal aggregates and display disrupted morphology

abnormal subiculum morphology
- neurons in subiculum are very pale, or absent

amyloid beta deposits
- amyloid deposition increases rapidly with increasing age
- mice show Abeta₄₂ deposits at 2 months of age; Abeta₄₀ levels are lower in amyloid deposits; mice show robust intraneuronal amyloid deposition
- plaques appear first in deep cortical layers and in subiculum, and spread with age to fill most of cortex, subiculum and hippocampus; also, less numerous deposits are observed in thalamus, brainstem and olfactory bulb in older mice

astrocytosis

brain inflammation
- transgenic mice display neuroinflammation

decreased cerebral cortex pyramidal cell number
- large neurons in cortical layer 5 are reduced in number

gliosis
- microgliosis and astrogliosis is seen in plaque-bearing regions of the brain by 2 months of age; numbers of activated astrocytes and microglia increases with age

neurodegeneration
- synapse degeneration begins at 4 months of age, compared to nontransgenic controls, as shown by reduction in levels of synaptic markers; neurodeneration marker p25 level is ~150% of control at 9 and 12 months

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/?
involves: 129S4/SvJae * C57BL/6 * SJL

homeostasis/metabolism phenotype

amyloid beta deposits

mortality/aging

premature death
- impaired survival compared to wild-type mice
- survive longer than transgenic mice that are also Apoa4 null

nervous system phenotype

amyloid beta deposits

neuron degeneration

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
involves: C57BL/6 * C57BL/6J * CBA * SJL

homeostasis/metabolism phenotype

amyloid beta deposits

mortality/aging

premature death
- decreased survival at 10 months of age

nervous system phenotype

amyloid beta deposits

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/?
involves: C57BL/6 * SJL

behavior/neurological phenotype

abnormal response to novel object
- poor novel object recognition

impaired contextual conditioning behavior
- decreased % of time freezing in contextual fear conditioning test

impaired cued conditioning behavior
- decreased % of time freezing in cued fear conditioning test

hematopoietic system phenotype

increased microglial cell activation
- increased percentage of activated microglia as compared to controls

homeostasis/metabolism phenotype

amyloid beta deposits
- high levels of Abeta₄₂ and Abeta₄₀ in the hippocampus as compared to mice that also carry Cdk5r1^tm2.1Lht
- increased plaque load and size as compared to controls

immune system phenotype

increased microglial cell activation
- increased percentage of activated microglia as compared to controls

nervous system phenotype

abnormal astrocyte physiology
- increased percentage of reactive astrocytes as compared to controls

abnormal long term depression
- decreased magnitude of long term depression as compared to controls

amyloid beta deposits
- high levels of Abeta₄₂ and Abeta₄₀ in the hippocampus as compared to mice that also carry Cdk5r1^tm2.1Lht
- increased plaque load and size as compared to controls

increased microglial cell activation
- increased percentage of activated microglia as compared to controls

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
B6SJL-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/Mmjax

homeostasis/metabolism phenotype

amyloid beta deposits
- retinal amyloid beta accumulates in the retinal pigment epithelial (RPE) layer and amyloid beta deposits are seen beneath the RPE layer

nervous system phenotype

amyloid beta deposits
- retinal amyloid beta accumulates in the retinal pigment epithelial (RPE) layer and amyloid beta deposits are seen beneath the RPE layer

pigmentation phenotype

abnormal retinal pigment epithelium morphology
- abundant intracellular amyloid beta is seen in the cytosol of RPE and with increasing intracellular accumulation of amyloid beta, tight junction integrity is attenuated and disorganized

abnormal retinal pigmentation
- 12 month old mutants show hypopigmentation in the RPE layer

vision/eye phenotype

abnormal Bruch membrane morphology
- thickened Bruch membrane is seen in the retina of 12 month old mutants

abnormal eye morphology
- drusen-like deposit is seen between the retinal pigment epithelium (RPE) layer and Bruch membrane in 12 month old mutants

abnormal retina morphology
- large vacuoles are seen in the retina of 12 month old mutants

abnormal retinal pigment epithelium morphology
- abundant intracellular amyloid beta is seen in the cytosol of RPE and with increasing intracellular accumulation of amyloid beta, tight junction integrity is attenuated and disorganized

abnormal retinal pigmentation
- 12 month old mutants show hypopigmentation in the RPE layer

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
involves: C57BL/6 * C57BL/6J * SJL

behavior/neurological phenotype

abnormal spatial reference memory
- during the hidden platform trials of the Morris water maze, mice show deficiency in memorizing the platform location
- Normal - mice subjected to 16 weeks of voluntary running exercise show improved performance in the Morris water maze during the hidden platform trials
- Normal - mice treated with ML246 for 5 weeks show improved performance in the Morris water maze during the hidden platform trials

homeostasis/metabolism phenotype

amyloid beta deposits
- Normal - 6 month old mice treated with ML246, a brain-penetrable autophagy-inducing small molecule, for 5 weeks show decreased levels of both soluble and insoluble amyloid beta 42 in the brain and a trend in plaque reduction, especially in the cerebral cortex
- Normal - however, expression of the precursor APP is unaffected in ML246 treated mice
- mice exhibit increased levels of both soluble and insoluble amyloid beta 42 in the brain
- Normal - mice subjected to 16 weeks of voluntary running have lower levels of both soluble and insoluble amyloid beta 42 in brain and show a reduction of amyloid plaques than mice housed without running wheels, indicating that physical activity decreases amyloid burden

nervous system phenotype

amyloid beta deposits
- Normal - 6 month old mice treated with ML246, a brain-penetrable autophagy-inducing small molecule, for 5 weeks show decreased levels of both soluble and insoluble amyloid beta 42 in the brain and a trend in plaque reduction, especially in the cerebral cortex
- Normal - however, expression of the precursor APP is unaffected in ML246 treated mice
- mice exhibit increased levels of both soluble and insoluble amyloid beta 42 in the brain
- Normal - mice subjected to 16 weeks of voluntary running have lower levels of both soluble and insoluble amyloid beta 42 in brain and show a reduction of amyloid plaques than mice housed without running wheels, indicating that physical activity decreases amyloid burden

The following phenotype relates to a compound genotype created using this strain

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
B6.Cg-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

behavior/neurological phenotype

decreased anxiety-related response
- increased open to total arm entry ratio in 5 month old females, however, phenotype is more severe in homozygotes

limb grasping
- increased clasping during tail suspension in 5 month old females as compared to controls, however clasping in homozygotes is more severe

growth/size/body region phenotype

decreased body weight
- reduced body weight at 2 months old females, but weight is similar to control by 5 months of age

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas
B6.Cg-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

behavior/neurological phenotype

abnormal posture
- postural abnormalities observed in 9 month old males

abnormal spatial reference memory
- impaired spacial reference memory in 5 month old females

decreased anxiety-related response
- increased open to total arm entry ratio in 2 and 5 month old females
- loss of normal anxiety phenotype

impaired balance
- 9 month old males either remain still on balance beam or fall off due to hind limb paresis
- impairment in balance and general motor coordination in 5 month old females as measured by the balance beam
- poor performance in string suspension paradigm as compared to wild-type and female hemizygotes at 5 months of age

impaired coordination
- impairment in balance and general motor coordination in 5 month old females as measured by the balance beam

impaired spatial learning
- impaired acquisition in 2 and 5 month old females; escape latencies increase over 5 days of training

impaired swimming
- decreased average swimming speed during cued training in 5 month old females, however no difference in day 3 escape latency

limb grasping
- increased clasping behavior during tail suspension in 5 month old females

paresis
- hind limb paresis in 9 month old males

pup cannibalization
- in females older than 5 months of age

growth/size/body region phenotype

cachexia
- wasting observed in 9 month old males

decreased body weight
- reduced body weight in 2 and 5 month old females

homeostasis/metabolism phenotype

amyloid beta deposits
- increase in plaque load in spinal cord of 9 month old males
- increased extracellular plaque load and intracellular Abeta immunoreacitivy in large spinal cord neurons in 9 month old males
- increased plaque load in cortex, hippocampus and thalamus at 2 (females), 5 (females) and 9 (males) months
- increased SDS-soluble Abeta_1-42 levels at 2 and 5 months (females) as compared to hemizygotes
- increased TBS-soluble Abeta_1-42 and Abeta_1-40 levels at 2 and 5 months (females) as compared to hemizygotes

nervous system phenotype

amyloid beta deposits
- increase in plaque load in spinal cord of 9 month old males
- increased extracellular plaque load and intracellular Abeta immunoreacitivy in large spinal cord neurons in 9 month old males
- increased plaque load in cortex, hippocampus and thalamus at 2 (females), 5 (females) and 9 (males) months
- increased SDS-soluble Abeta_1-42 levels at 2 and 5 months (females) as compared to hemizygotes
- increased TBS-soluble Abeta_1-42 and Abeta_1-40 levels at 2 and 5 months (females) as compared to hemizygotes

axonal spheroids
- increase in axonal swellings in pons and gray matter of spinal cord of 9 month old male homozygotes as compared to hemizygotes

reproductive system phenotype

decreased litter size
- in females older than 5 months of age

References

Oakley H; Cole SL; Logan S; Maus E; Shao P; Craft J; Guillozet-Bongaarts A; Ohno M; Disterhoft J; Van Eldik L; Berry R; Vassar R. 2006. Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. J Neurosci 26(40):10129-40PubMed: 17021169 MGI: J:112949

Additional References

Ulland TK; Song WM; Huang SC; Ulrich JD; Sergushichev A; Beatty WL; Loboda AA; Zhou Y; Cairns NJ; Kambal A; Loginicheva E; Gilfillan S; Cella M; Virgin HW; Unanue ER; Wang Y; Artyomov MN; Holtzman DM; Colonna M. 2017. TREM2 Maintains Microglial Metabolic Fitness in Alzheimer's Disease. Cell 170(4):649-663.e13PubMed: 28802038 MGI: J:242830
Dukhinova M; Veremeyko T; Yung AWY; Kuznetsova IS; Lau TYB; Kopeikina E; Chan AML; Ponomarev ED. 2019. Fresh evidence for major brain gangliosides as a target for the treatment of Alzheimer's disease. Neurobiol Aging 77:128-143PubMed: 30797170 MGI: J:281541

Additional - Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas related

Technical Support

Contact Technical Support

Genotyping Protocols
- QPCR:Tg(APP)-qPCR
- Standard PCR:Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas-Chr3
- Probe:Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas-Chr3-Probe
- Probe:Tg(APP)-qPCR
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, hemizygous mice may be bred to C57BL/6J mice.
- Additional Breeding and Husbandry Support
Mating System
- Hemizygous x C57BL/6J (000664)
- C57BL/6J (000664) x Hemizygous
Citation
When using the B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax mouse strain in a publication, please cite the originating article(s) and include MMRRC stock #34848 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX12 (Maximum)

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Questions about Terms of Use

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Licensing Information

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Email: TechTran@jax.org

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Also Known As: 5XFAD

Donating Investigator

Genetic overview

Research Applications

Detailed Description

Development

Expression Data

Control Suggestions

Additional Information

Selected References

Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas

Allele Symbol: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Mammalian Phenotype Terms by Genotype

Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0involves: C57BL/6 * SJL

behavior/neurological phenotype

homeostasis/metabolism phenotype

immune system phenotype

nervous system phenotype

Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/?involves: 129S4/SvJae * C57BL/6 * SJL

homeostasis/metabolism phenotype

mortality/aging

nervous system phenotype

Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0involves: C57BL/6 * C57BL/6J * CBA * SJL

homeostasis/metabolism phenotype

mortality/aging

nervous system phenotype

Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/?involves: C57BL/6 * SJL

behavior/neurological phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

nervous system phenotype

Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax

homeostasis/metabolism phenotype

nervous system phenotype

pigmentation phenotype

vision/eye phenotype

Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0involves: C57BL/6 * C57BL/6J * SJL

behavior/neurological phenotype

homeostasis/metabolism phenotype

nervous system phenotype

Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas

behavior/neurological phenotype

growth/size/body region phenotype

Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Tg(APPSwFlLon,PSEN1*M146L*L286V)6799VasB6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas

behavior/neurological phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

nervous system phenotype

reproductive system phenotype

References

Additional References

Additional - Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

The Jackson Laboratory's Genotype Promise

Terms of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Allele Symbol: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
involves: C57BL/6 * SJL

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/?
involves: 129S4/SvJae * C57BL/6 * SJL

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
involves: C57BL/6 * C57BL/6J * CBA * SJL

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/?
involves: C57BL/6 * SJL

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
B6SJL-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/Mmjax

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
involves: C57BL/6 * C57BL/6J * SJL

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/0
B6.Cg-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Genotype: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas/Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas
B6.Cg-Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Additional - Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas related