Overview

Also Known As:5XFAD, Tg6799

These 5XFAD transgenic mice overexpress mutant human amyloid beta (A4) precursor protein 695 (APP) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations along with human presenilin 1 (PS1) harboring two FAD mutations, M146L and L286V. Both transgenes are regulated by the mouse Thy1 promoter to drive overexpression in the brain. 5XFAD mice recapitulate major features of Alzheimer's Disease amyloid pathology and may be a useful model of intraneuronal Abeta-42 induced neurodegeneration and amyloid plaque formation.

Donating Investigator

Robert Vassar, Northwestern University

Genetic overview

Genetic Background	Generation
100012 B6SJLF1/J	N11+N26 (2020-04-28 00:00:00)

Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Allele Type
Transgenic (Inserted expressed sequence, Humanized sequence)

View Genetics

Research Applications

Mouse/Human Gene Homologs
Neurobiology Research
Research Tools

View All Research Applications

Details

Important Note

Because this model is maintained by backcrossing transgenic animals to a B6SJLF1 hybrid at every generation, C57BL/6J and SJL/J content is segregating in the progeny of these animals. Mice produced from this cross could be genotypically heterozygous, homozygous or wildtype for mutations including the age related hearing loss 1 allele Cdh23^ahl, the retinal degeneration allele Pde6b^rd1, the Trem2^S148E allele, etc.

Detailed Description

These 5XFAD transgenic mice overexpress both mutant human amyloid beta (A4) precursor protein 695 (APP) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations and human presenilin 1 (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 6799 founder line have high APP expression correlating with high burden and accelerated accumulation of the 42 amino acid species of beta-amyloid (Abeta-42). 5XFAD mice generate Abeta-42 almost exclusively, rapidly accumulating massive cerebral levels. On this mixed C57BL/6 and SJL background (MMRRC stock 34840), intraneuronal Abeta-42 accumulation is observed starting at 1.5 months of age in hemizygotes, 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 in hemizygotes is not as robust as that demonstrated in hemizygotes from the mixed C57BL/6 and SJL background (view data). In addition, these mice have reduced synaptic marker protein levels, increased p25 (formally Cdk5) levels, neuron loss, reduced anxiety, poor novel object recognition, impaired conditioned behavior and memory impairment in the Y-maze test. 5XFAD males exhibit increased home cage aggression and decreased social investigation in both males and females. 5XFAD transgenic mice recapitulate major features of Alzheimer's Disease amyloid pathology and may be useful models of intraneuronal Abeta-42 induced neurodegeneration and amyloid plaque formation. Hemizygous mice are viable and fertile.

This strain is segregating heterozygous/wildtype for the retinal degeneration allele Pde6b^rd1.

It should be noted that the SJL genetic background contains the Trem2^S148E allele - a naturally occurring variant at position 48351151-48351152 on Chr 17 (rs108080490 and rs107649577; Ensembl GRCm38.p6). This TC to GA transition results in a serine to glutamic acid substitution at amino acid 148 (S148E). Because this model (MMRRC stock 34840) is maintained by backcrossing transgenic animals to a B6SJLF1 hybrid at every generation, SJL content is segregating in the progeny of these animals. Mice produced from this cross could be genotypically heterozygous, homozygous or wildtype for this Trem2^S148E. This variant may be of particular interest to those studying the role played by TREM2 (triggering receptor expressed on myeloid cells 2) in Alzheimer's Disease pathology.

NOTE: This 5XFAD transgene is also available on a C57BL/6J background (see MMRRC stock 34848), which does not carry the Trem2^S148E allele.

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 "C57BL/6XSJL" hybrid embryos. Founders from the highest APP expressing line (Tg6799) were bred with (B6SJL)F1 mice for more than 10 generations with stable germ-line transmission and expression of both transgenes, demonstrating that these "5XFAD"; mice breed as single transgenics. 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

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)	5XFAD; 5XFAD APP/PS1; 5XFAD line Tg6799; Tg(APPSweFlLon,PSEN1M146L*L286V)6799Vas; Tg-5xFAD; Tg6799
Gene Symbol and Name	Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas, transgene insertion 6799, Robert Vassar
Gene Synonym(s)
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 Phenotype

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

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

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

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
- increased plaque load in cortex, hippocampus and thalamus at 2 (females), 5 (females) and 9 (males) months
- increased TBS-soluble Abeta_1-42 and Abeta_1-40 levels at 2 and 5 months (females) as compared to hemizygotes
- 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 SDS-soluble Abeta_1-42 levels at 2 and 5 months (females) as compared to hemizygotes

nervous system phenotype

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

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

behavior/neurological phenotype

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

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

abnormal posture
- postural abnormalities observed in 9 month old males

pup cannibalization
- in females older than 5 months of age

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

paresis
- hind limb paresis in 9 month old males

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

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

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

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

behavior/neurological phenotype

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

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

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

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

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

nervous system 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

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

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

behavior/neurological phenotype

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

abnormal response to novel object
- poor novel object recognition

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

immune system phenotype

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

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

nervous system phenotype

amyloid beta deposits
- mice exhibit increased levels of both soluble and insoluble amyloid beta 42 in the brain
- 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
- 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

behavior/neurological phenotype

abnormal spatial reference memory
- Normal - mice subjected to 16 weeks of voluntary running exercise show improved performance in the Morris water maze during the hidden platform trials
- during the hidden platform trials of the Morris water maze, mice show deficiency in memorizing the platform location
- 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
- 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
- Normal - however, expression of the precursor APP is unaffected in ML246 treated mice

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 retina morphology
- large vacuoles are 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 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 * 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 subiculum morphology
- neurons in subiculum are very pale, or absent

amyloid beta deposits
- 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
- 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

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

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

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

brain inflammation
- transgenic mice display neuroinflammation

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

astrocytosis

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

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

Creighton SD; Mendell AL; Palmer D; Kalisch BE; MacLusky NJ; Prado VF; Prado MAM; Winters BD. 2019. Dissociable cognitive impairments in two strains of transgenic Alzheimer's disease mice revealed by a battery of object-based tests. Sci Rep 9(1):57PubMed: 30635592 MGI: J:275422
Gail Canter R; Huang WC; Choi H; Wang J; Ashley Watson L; Yao CG; Abdurrob F; Bousleiman SM; Young JZ; Bennett DA; Delalle I; Chung K; Tsai LH. 2019. 3D mapping reveals network-specific amyloid progression and subcortical susceptibility in mice. Commun Biol 2:360PubMed: 31602409 MGI: J:284807
Gur E; Fertan E; Alkins K; Wong AA; Brown RE; Balci F. 2019. Interval timing is disrupted in female 5xFAD mice: An indication of altered memory processes. J Neurosci Res 97(7):817-827PubMed: 30973189 MGI: J:285563
Kosel F; Hamilton JS; Harrison SL; Godin V; Franklin TB. 2020. Reduced social investigation and increased injurious behavior in transgenic 5xFAD mice. J Neurosci ResPubMed: 31912571 MGI: J:285946
Park SW; Kim JH; Mook-Jung I; Kim KW; Park WJ; Park KH; Kim JH. 2014. Intracellular amyloid beta alters the tight junction of retinal pigment epithelium in 5XFAD mice. Neurobiol Aging 35(9):2013-20PubMed: 24709310 MGI: J:214858
Rocchi A; Yamamoto S; Ting T; Fan Y; Sadleir K; Wang Y; Zhang W; Huang S; Levine B; Vassar R; He C. 2017. A Becn1 mutation mediates hyperactive autophagic sequestration of amyloid oligomers and improved cognition in Alzheimer's disease. PLoS Genet 13(8):e1006962PubMed: 28806762 MGI: J:244104
Seo J; Giusti-Rodriguez P; Zhou Y; Rudenko A; Cho S; Ota KT; Park C; Patzke H; Madabhushi R; Pan L; Mungenast AE; Guan JS; Delalle I; Tsai LH. 2014. Activity-Dependent p25 Generation Regulates Synaptic Plasticity and Abeta-Induced Cognitive Impairment. Cell 157(2):486-98PubMed: 24725413 MGI: J:208030
Zhao J; Fu Y; Yasvoina M; Shao P; Hitt B; O'Connor T; Logan S; Maus E; Citron M; Berry R; Binder L; Vassar R. 2007. Beta-site amyloid precursor protein cleaving enzyme 1 levels become elevated in neurons around amyloid plaques: implications for Alzheimer's disease pathogenesis. J Neurosci 27(14):3639-49PubMed: 17409228 MGI: J:119403

Additional - Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Generic Pde6b
- Standard PCR:Generic Pde6b Alternate1
- Probe:Pde6b Probe
- Standard PCR:Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas-Chr3
- Sanger sequencing:Trem2 rs107649577-SEQ
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, hemizygous mice may be bred to B6SJLF1/J (Stock No. 100012).
- Additional Breeding and Husbandry Support
Mating System
- Hemizygote x F1
- F1 x Hemizygote
Appearance
- multiple coat colors
  Related Genotype: segregating for a, A, Oca2^p, Tyr^c and Pde6b^rd1
Citation
When using the 5XFAD mouse strain in a publication, please cite the originating article(s) and include MMRRC stock #34840 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Terms Of Use

General Terms and Conditions

See MMRRC for Additional Conditions of Distribution

Questions about Terms of Use

Additional Use Restrictions Apply

Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:5XFAD, Tg6799

Donating Investigator

Genetic overview

Research Applications

Important Note

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 Phenotype

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 * C57BL/6J * CBA * SJL

homeostasis/metabolism phenotype

mortality/aging

nervous system phenotype

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

growth/size/body region phenotype

homeostasis/metabolism phenotype

nervous system phenotype

reproductive system phenotype

behavior/neurological 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/?involves: C57BL/6 * SJL

nervous system phenotype

behavior/neurological phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

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

nervous system phenotype

behavior/neurological phenotype

homeostasis/metabolism 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 * SJL

behavior/neurological phenotype

homeostasis/metabolism phenotype

immune system phenotype

nervous system phenotype

References

Additional References

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

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

Allele Symbol: Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas

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

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

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

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

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

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

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

Additional - Tg(APPSwFlLon,PSEN1M146LL286V)6799Vas related