Strain Name:

B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2Mmjax

Availability:

Repository- Live     Available at the JAX MMRRC

Use Restrictions Apply, see Terms of Use
Common Names: J20 line;    
This strain is now distributed by the Mutant Mouse Regional Resource Center. Please refer to the Mutant Mouse Regional Resource Center (MMRRC) for ordering information and strain details on B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J/Mmjax MMRRC Stock Number 034836.
As a designated MMRRC center, The Jackson Laboratory will continue to distribute these mice at the same high health and
quality standards but ordering is exclusively provided through the MMRRC.
These transgenic mice (formerly JAX Stock No. 006293) express a mutant form of the human amyloid protein precursor bearing both the Swedish (K670N/M671L) and the Indiana (V717F) mutations (APPSwInd). They show progressive amyloid deposition as they age. This mutant mouse strain represents a model that may be useful in studies of the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.

Description

Strain Information

Former Names B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J    (Changed: 11-AUG-11 )
Type Congenic; Mutant Strain; Transgenic;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Mating SystemInbred x Hemizygote         (Female x Male)   28-OCT-13
Specieslaboratory mouse
GenerationN12+N14 (09-OCT-12)
Generation Definitions
 
Donating Investigator Lennart Mucke,   Gladstone Inst of Neurological Disease

Important Note
In March 2010, the donating investigator performed quantitative PCR on genomic DNA and determination of amyloid-beta levels in brain extract from the JAX Stock No. 006293 distribution colony (B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J also called "J20" line). Results of these analyses demonstrate that the current distribution colony maintains similar transgene copy number and expression as previously published (Mucke et. al. J Neurosci. 2000 Jun 1; 20(11): 4050-8).

Description
These transgenic mice express a mutant form of the human amyloid protein precursor bearing both the Swedish (K670N/M671L) and the Indiana (V717F) mutations (APPSwInd). Expression of the transgenic insert is directed by the human platelet-derived growth factor beta polypeptide (PDGFB) promoter. Hemizygotes express immunodetectable transgene product in cerebral neurons, with the highest level of expression occurring in the neocortex and hippocampus. Enzyme-linked immunosorbent assay (ELISA) analysis reveals approximate total amyloid beta peptides and 42 amino acid length amyloid beta peptides in neocortical and hippocampal tissue from mutant mice. At five to seven months of age diffuse amyloid beta peptides deposition in the dendate gyrus and neocortex forms. Amyloid deposition is progressive with all transgenic mice exhibiting plaques by age eight to 10 months. Pups born of carrier females have shown an increased mortality rate in our colonies. The Donating Researcher has observed an approximately 15% mortality rate in the first 6 months of life. Video-EEG monitoring of 4 to 7 month old hemizygous transgenic mice, N10+ on the C57BL/6J background, reveals hippocampal hyperexcitability and cortical and hippocampal spontaneous nonconvulsive seizures. The mice are immobile, with no myoclonic behavior observed, during the non-convulsive electroencephalographic seizures. Pentylenetetrazole induced seizures have earlier onset, are more severe and result in more frequent deaths (50% develop fatal status epilepticus) than wildtype controls (Palop et al. Neuron 2007). This mutant mouse strain represents a model that may be useful in studies of the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.

Development
A transgenic construct containing the mutant human amyloid protein precursor APPSwInd under the control of human platelet-derived growth factor beta polypeptide, simian sarcoma viral (v-sis) oncogene homolog, (PDGFB) promoter, was injected into C57BL/6 X DBA/2 F2 one-cell embryos. Heterozygous founder animals were bred to C57BL/6 X DBA/2 F1 mice. The resulting transgenic mice were then backcrossed for 12 generations on the C57BL/6J background.

This strain was previously distributed as B6.Cg-Tg(PDGFB-APPSwInd)20Lms/1J. That strain was found to have undergone a loss of transgenic copy number and consequent delayed onset of the phenotype, so this strain was re-imported from the lab of Dr. Lennart Mucke. Transgenic copy number is assayed using a Multiplex TaqMan assay.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

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View Alzheimer's Disease Models     (109 strains)

View Strains carrying other alleles of APP     (16 strains)

View Strains carrying other alleles of PDGFB     (5 strains)

Additional Web Information

Visit the Alzheimer's Disease Mouse Model Resource site for helpful information on Alzheimer's Disease and research resources.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.
Alzheimer Disease; AD
- Potential model based on transgenic expression of an ortholog of a human gene that is associated with this disease. Phenotypic similarity to the human disease has not been tested.
Cerebral Amyloid Angiopathy, App-Related   (APP)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tg(PDGFB-APPSwInd)20Lms/0

        B6.D2-Tg(PDGFB-APPSwInd)20Lms
  • nervous system phenotype
  • abnormal neuron morphology
    • dystrophic neurites are associated with plaques   (MGI Ref ID J:100954)
  • amyloid beta deposits
    • mice develop amyloid peptide deposits by 5-7 months of age   (MGI Ref ID J:100954)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits
    • mice develop amyloid peptide deposits by 5-7 months of age   (MGI Ref ID J:100954)

Tg(PDGFB-APPSwInd)20Lms/0

        B6.Cg-Tg(PDGFB-APPSwInd)20Lms
  • nervous system phenotype
  • abnormal cerebral cortex pyramidal cell morphology
    • at 6 months and 12 to 16 months of age, 30% fewer pyramidal cells in the entorhinal cortex express Reelin than in wild-type mice   (MGI Ref ID J:118589)
    • however, no neuron loss is observed   (MGI Ref ID J:118589)

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

Tg(PDGFB-APPSwInd)20Lms/0

        involves: C57BL/6 * DBA/2
  • mortality/aging
  • premature death   (MGI Ref ID J:141084)
    • mice show premature death of unclear etiology with >15% mortality exhibited by 6 months, compared to all other genotypes   (MGI Ref ID J:121330)
    • high rate of premature (6 months or earlier) death   (MGI Ref ID J:87150)
  • behavior/neurological phenotype
  • abnormal long term object recognition memory
    • at 4-7 months of age, mice transgenic mice with wild-type Mapt expression take longer to locate the platform in the cued version of the Morris water maze test compared to transgenic mice heterozygous or homozygous for Mapt deletion   (MGI Ref ID J:121330)
  • abnormal spatial learning
    • in the hidden platform version of the Morris water maze, non-trangenic controls, regardless of Mapt genotype learn the task over 3 days, whereas transgenic mice with wild-type expression of Mapt show no evidence of learning   (MGI Ref ID J:121330)
    • in probe trials where the platform is removed, mice show no learning, displaying no significantly elevated crossings of the target quadrant after 5 days of training   (MGI Ref ID J:121330)
    • in a Morris water maze, mice fail to favor the target platform location unlike wild-type mice   (MGI Ref ID J:141084)
  • decreased anxiety-related response
    • mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice   (MGI Ref ID J:141084)
  • hyperactivity   (MGI Ref ID J:141084)
    • mice show hyperactivity in the Y-maze, a new cage, and elevated-plus maze compared to other transgenic mice or non-transgenic controls; this persists in mice 12-16 months of age   (MGI Ref ID J:121330)
  • increased susceptibility to pharmacologically induced seizures
    • mice are abnormally sensitive to pentylenetetrazole (PTZ)-induced seizures with 20% suffering fatal status epilepticus at a PTZ dose not lethal in non-transgenic controls   (MGI Ref ID J:121330)
  • nervous system phenotype
  • abnormal neuron morphology
    • mice show neuritic dystrophy around amyloid plaques   (MGI Ref ID J:121330)
    • abnormal neuron differentiation
      • aberrant sprouting of hippocampal axons is observed in transgenic mice   (MGI Ref ID J:121330)
  • amyloid beta deposits
    • diffuse immunoreactive amyloid deposits detected in dentate gyrus and neocortex of mice aged 5 to 7 months old   (MGI Ref ID J:62290)
    • all mice exhibit plaques by age 8 to 10 months   (MGI Ref ID J:62290)
    • at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous null for Mapt   (MGI Ref ID J:121330)
    • soluble and insoluble Abeta-40 and -42 peptide deposits at 6-10 months   (MGI Ref ID J:87150)
  • increased susceptibility to pharmacologically induced seizures
    • mice are abnormally sensitive to pentylenetetrazole (PTZ)-induced seizures with 20% suffering fatal status epilepticus at a PTZ dose not lethal in non-transgenic controls   (MGI Ref ID J:121330)
  • neurodegeneration
    • neurodegeneration is indicated by an age dependent decrease in density of synaptophysin-immunoreactive presynaptic terminals   (MGI Ref ID J:62290)
  • cellular phenotype
  • abnormal neuron differentiation
    • aberrant sprouting of hippocampal axons is observed in transgenic mice   (MGI Ref ID J:121330)
  • homeostasis/metabolism phenotype
  • amyloid beta deposits
    • diffuse immunoreactive amyloid deposits detected in dentate gyrus and neocortex of mice aged 5 to 7 months old   (MGI Ref ID J:62290)
    • all mice exhibit plaques by age 8 to 10 months   (MGI Ref ID J:62290)
    • at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous null for Mapt   (MGI Ref ID J:121330)
    • soluble and insoluble Abeta-40 and -42 peptide deposits at 6-10 months   (MGI Ref ID J:87150)
View Research Applications

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

Neurobiology Research
Alzheimer's Disease
      strains expressing mutant APP
Behavioral and Learning Defects
Epilepsy
      electroconvulsive seizures
      increased susceptibility to kainate-induced seizures

APP related

Neurobiology Research
Neurodegeneration

Tg(PDGFB-APPSwInd)20Lms related

Neurobiology Research
Alzheimer's Disease

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tg(PDGFB-APPSwInd)20Lms
Allele Name transgene insertion 20, Lennart Mucke
Allele Type Transgenic (Inserted expressed sequence)
Common Name(s) APP Tg; APP/J20; J20; PDAPP-J20; PDGF-APPSwInd; PDGF-hAPP695,751,770V171F, KM670/671NL; hAPPJ20;
Mutation Made By Lennart Mucke,   Gladstone Inst of Neurological Disease
Strain of Origin(C57BL/6 x DBA/2)F2
Expressed Gene APP, amyloid beta (A4) precursor protein, human
Promoter PDGFB, platelet-derived growth factor beta polypeptide, human
General Note This line is also called line J20.

Diffuse amyloid beta peptides deposition forms in the dendate gyrus and neocortex at 5 to 7 months of age. Amyloid deposition is progressive, with all transgenic mice exhibiting plaques by age 8 to 10 months.

Molecular Note The transgene expresses the mutant human amyloid protein precursor APPSwInd, which bears both the Swedish (K670N/M671L) and the Indiana (V717F) mutations, under the control of the human platelet derived growth factor, B polypeptide (PDGFB) promoter. Hemizygous transgenic mice express immunodetectable transgene product in cerebral neurons, with the highest level of expression occurring in the neocortex and hippocampus. ELISA analysis reveals approximate total amyloid beta peptides and 42 amino acid lengthamyloid beta peptides in neocortical and hippocampal tissue from transgenic mice. [MGI Ref ID J:62290]
 
 

Genotyping

Genotyping Information

Genotyping Protocols

Tg(APP), QPCR
Tg(PDGFB-APP), Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Mucke L; Masliah E; Yu GQ; Mallory M; Rockenstein EM; Tatsuno G; Hu K; Kholodenko D; Johnson-Wood K; McConlogue L. 2000. High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation. J Neurosci 20(11):4050-8. [PubMed: 10818140]  [MGI Ref ID J:62290]

Additional References

Moreno H; Wu WE; Lee T; Brickman A; Mayeux R; Brown TR; Small SA. 2007. Imaging the abeta-related neurotoxicity of Alzheimer disease. Arch Neurol 64(10):1467-77. [PubMed: 17923630]  [MGI Ref ID J:125332]

Tg(PDGFB-APPSwInd)20Lms related

Aucoin JS; Jiang P; Aznavour N; Tong XK; Buttini M; Descarries L; Hamel E. 2005. Selective cholinergic denervation, independent from oxidative stress, in a mouse model of Alzheimer's disease. Neuroscience 132(1):73-86. [PubMed: 15780468]  [MGI Ref ID J:97281]

Baron R; Harpaz I; Nemirovsky A; Cohen H; Monsonego A. 2007. Immunity and neuronal repair in the progression of Alzheimer's disease: a brief overview. Exp Gerontol 42(1-2):64-9. [PubMed: 17074458]  [MGI Ref ID J:123181]

Baron R; Nemirovsky A; Harpaz I; Cohen H; Owens T; Monsonego A. 2008. IFN-gamma enhances neurogenesis in wild-type mice and in a mouse model of Alzheimer's disease. FASEB J 22(8):2843-52. [PubMed: 18390924]  [MGI Ref ID J:138024]

Beauquis J; Pavia P; Pomilio C; Vinuesa A; Podlutskaya N; Galvan V; Saravia F. 2013. Environmental enrichment prevents astroglial pathological changes in the hippocampus of APP transgenic mice, model of Alzheimer's disease. Exp Neurol 239:28-37. [PubMed: 23022919]  [MGI Ref ID J:196994]

Belkacemi A; Ramassamy C. 2012. Time sequence of oxidative stress in the brain from transgenic mouse models of Alzheimer's disease related to the amyloid-beta cascade. Free Radic Biol Med 52(3):593-600. [PubMed: 22172527]  [MGI Ref ID J:180298]

Bien-Ly N; Andrews-Zwilling Y; Xu Q; Bernardo A; Wang C; Huang Y. 2011. C-terminal-truncated apolipoprotein (apo) E4 inefficiently clears amyloid-beta (Abeta) and acts in concert with Abeta to elicit neuronal and behavioral deficits in mice. Proc Natl Acad Sci U S A 108(10):4236-41. [PubMed: 21368138]  [MGI Ref ID J:170827]

Bien-Ly N; Gillespie AK; Walker D; Yoon SY; Huang Y. 2012. Reducing human apolipoprotein E levels attenuates age-dependent Abeta accumulation in mutant human amyloid precursor protein transgenic mice. J Neurosci 32(14):4803-11. [PubMed: 22492035]  [MGI Ref ID J:184138]

Buckwalter MS; Coleman BS; Buttini M; Barbour R; Schenk D; Games D; Seubert P; Wyss-Coray T. 2006. Increased T cell recruitment to the CNS after amyloid beta 1-42 immunization in Alzheimer's mice overproducing transforming growth factor-beta 1. J Neurosci 26(44):11437-41. [PubMed: 17079673]  [MGI Ref ID J:114703]

Caspersen C; Wang N; Yao J; Sosunov A; Chen X; Lustbader JW; Xu HW; Stern D; McKhann G; Yan SD. 2005. Mitochondrial Abeta: a potential focal point for neuronal metabolic dysfunction in Alzheimer's disease. FASEB J 19(14):2040-1. [PubMed: 16210396]  [MGI Ref ID J:127883]

Cheng IH; Palop JJ; Esposito LA; Bien-Ly N; Yan F; Mucke L. 2004. Aggressive amyloidosis in mice expressing human amyloid peptides with the Arctic mutation. Nat Med 10(11):1190-2. [PubMed: 15502844]  [MGI Ref ID J:100954]

Cheng IH; Scearce-Levie K; Legleiter J; Palop JJ; Gerstein H; Bien-Ly N; Puolivali J; Lesne S; Ashe KH; Muchowski PJ; Mucke L. 2007. Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. J Biol Chem 282(33):23818-28. [PubMed: 17548355]  [MGI Ref ID J:124712]

Cheng JS; Dubal DB; Kim DH; Legleiter J; Cheng IH; Yu GQ; Tesseur I; Wyss-Coray T; Bonaldo P; Mucke L. 2009. Collagen VI protects neurons against Abeta toxicity. Nat Neurosci 12(2):119-21. [PubMed: 19122666]  [MGI Ref ID J:145982]

Chin J; Massaro CM; Palop JJ; Thwin MT; Yu GQ; Bien-Ly N; Bender A; Mucke L. 2007. Reelin depletion in the Enthorhinal cortex of human amyloid precursor protein transgenic mice and humans with Alzheimer's disease J Neurosci 27(11):2727-2733. [PubMed: 17360894]  [MGI Ref ID J:118589]

Chin J; Palop JJ; Puolivali J; Massaro C; Bien-Ly N; Gerstein H; Scearce-Levie K; Masliah E; Mucke L. 2005. Fyn kinase induces synaptic and cognitive impairments in a transgenic mouse model of Alzheimer's disease. J Neurosci 25(42):9694-703. [PubMed: 16237174]  [MGI Ref ID J:102161]

Chin J; Palop JJ; Yu GQ; Kojima N; Masliah E; Mucke L. 2004. Fyn kinase modulates synaptotoxicity, but not aberrant sprouting, in human amyloid precursor protein transgenic mice. J Neurosci 24(19):4692-7. [PubMed: 15140940]  [MGI Ref ID J:96892]

Choi SW; Gerencser AA; Ng R; Flynn JM; Melov S; Danielson SR; Gibson BW; Nicholls DG; Bredesen DE; Brand MD. 2012. No consistent bioenergetic defects in presynaptic nerve terminals isolated from mouse models of Alzheimer's disease. J Neurosci 32(47):16775-84. [PubMed: 23175831]  [MGI Ref ID J:192812]

Cisse M; Halabisky B; Harris J; Devidze N; Dubal DB; Sun B; Orr A; Lotz G; Kim DH; Hamto P; Ho K; Yu GQ; Mucke L. 2011. Reversing EphB2 depletion rescues cognitive functions in Alzheimer model. Nature 469(7328):47-52. [PubMed: 21113149]  [MGI Ref ID J:167228]

Cisse M; Sanchez PE; Kim DH; Ho K; Yu GQ; Mucke L. 2011. Ablation of cellular prion protein does not ameliorate abnormal neural network activity or cognitive dysfunction in the j20 line of human amyloid precursor protein transgenic mice. J Neurosci 31(29):10427-31. [PubMed: 21775587]  [MGI Ref ID J:174512]

Davis AA; Fritz JJ; Wess J; Lah JJ; Levey AI. 2010. Deletion of M1 muscarinic acetylcholine receptors increases amyloid pathology in vitro and in vivo. J Neurosci 30(12):4190-6. [PubMed: 20335454]  [MGI Ref ID J:159221]

Deipolyi AR; Fang S; Palop JJ; Yu GQ; Wang X; Mucke L. 2008. Altered navigational strategy use and visuospatial deficits in hAPP transgenic mice. Neurobiol Aging 29(2):253-66. [PubMed: 17126954]  [MGI Ref ID J:130693]

Diaz-Hernandez JI; Gomez-Villafuertes R; Leon-Otegui M; Hontecillas-Prieto L; Del Puerto A; Trejo JL; Lucas JJ; Garrido JJ; Gualix J; Miras-Portugal MT; Diaz-Hernandez M. 2012. In vivo P2X7 inhibition reduces amyloid plaques in Alzheimer's disease through GSK3beta and secretases. Neurobiol Aging 33(8):1816-28. [PubMed: 22048123]  [MGI Ref ID J:196555]

Du H; Guo L; Yan S; Sosunov AA; McKhann GM; Yan SS. 2010. Early deficits in synaptic mitochondria in an Alzheimer's disease mouse model. Proc Natl Acad Sci U S A 107(43):18670-5. [PubMed: 20937894]  [MGI Ref ID J:165506]

Escribano L; Simon AM; Perez-Mediavilla A; Salazar-Colocho P; Del Rio J; Frechilla D. 2009. Rosiglitazone reverses memory decline and hippocampal glucocorticoid receptor down-regulation in an Alzheimer's disease mouse model. Biochem Biophys Res Commun 379(2):406-10. [PubMed: 19109927]  [MGI Ref ID J:144519]

Esposito L; Raber J; Kekonius L; Yan F; Yu GQ; Bien-Ly N; Puolivali J; Scearce-Levie K; Masliah E; Mucke L. 2006. Reduction in mitochondrial superoxide dismutase modulates Alzheimer's disease-like pathology and accelerates the onset of behavioral changes in human amyloid precursor protein transgenic mice. J Neurosci 26(19):5167-79. [PubMed: 16687508]  [MGI Ref ID J:108685]

Fang F; Chen X; Huang T; Lue LF; Luddy JS; Yan SS. 2012. Multi-faced neuroprotective effects of Ginsenoside Rg1 in an Alzheimer mouse model. Biochim Biophys Acta 1822(2):286-92. [PubMed: 22015470]  [MGI Ref ID J:180329]

Fisher Y; Nemirovsky A; Baron R; Monsonego A. 2010. T cells specifically targeted to amyloid plaques enhance plaque clearance in a mouse model of Alzheimer's disease. PLoS One 5(5):e10830. [PubMed: 20520819]  [MGI Ref ID J:160898]

Frost JL; Le KX; Cynis H; Ekpo E; Kleinschmidt M; Palmour RM; Ervin FR; Snigdha S; Cotman CW; Saido TC; Vassar RJ; George-Hyslop PS; Ikezu T; Schilling S; Demuth HU; Lemere CA. 2013. Pyroglutamate-3 Amyloid-beta Deposition in the Brains of Humans, Non-Human Primates, Canines, and Alzheimer Disease-Like Transgenic Mouse Models. Am J Pathol 183(2):369-81. [PubMed: 23747948]  [MGI Ref ID J:199082]

Gaikwad S; Larionov S; Wang Y; Dannenberg H; Matozaki T; Monsonego A; Thal DR; Neumann H. 2009. Signal regulatory protein-beta1: a microglial modulator of phagocytosis in Alzheimer's disease. Am J Pathol 175(6):2528-39. [PubMed: 19893026]  [MGI Ref ID J:155330]

Garcia-Barroso C; Ricobaraza A; Pascual-Lucas M; Unceta N; Rico AJ; Goicolea MA; Salles J; Lanciego JL; Oyarzabal J; Franco R; Cuadrado-Tejedor M; Garcia-Osta A. 2013. Tadalafil crosses the blood-brain barrier and reverses cognitive dysfunction in a mouse model of AD. Neuropharmacology 64:114-23. [PubMed: 22776546]  [MGI Ref ID J:192668]

Grand'maison M; Zehntner SP; Ho MK; Hebert F; Wood A; Carbonell F; Zijdenbos AP; Hamel E; Bedell BJ. 2013. Early cortical thickness changes predict beta-amyloid deposition in a mouse model of Alzheimer's disease. Neurobiol Dis 54:59-67. [PubMed: 23454197]  [MGI Ref ID J:197951]

Griffiths HH; Whitehouse IJ; Baybutt H; Brown D; Kellett KA; Jackson CD; Turner AJ; Piccardo P; Manson JC; Hooper NM. 2011. Prion Protein Interacts with BACE1 Protein and Differentially Regulates Its Activity toward Wild Type and Swedish Mutant Amyloid Precursor Protein. J Biol Chem 286(38):33489-500. [PubMed: 21795680]  [MGI Ref ID J:176738]

Gultner S; Laue M; Riemer C; Heise I; Baier M. 2009. Prion disease development in slow Wallerian degeneration (Wld(S)) mice. Neurosci Lett 456(2):93-8. [PubMed: 19429141]  [MGI Ref ID J:150443]

Harris JA; Devidze N; Halabisky B; Lo I; Thwin MT; Yu GQ; Bredesen DE; Masliah E; Mucke L. 2010. Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor protein. J Neurosci 30(1):372-81. [PubMed: 20053918]  [MGI Ref ID J:157639]

Hebert F; Grand'maison M; Ho MK; Lerch JP; Hamel E; Bedell BJ. 2013. Cortical atrophy and hypoperfusion in a transgenic mouse model of Alzheimer's disease. Neurobiol Aging 34(6):1644-52. [PubMed: 23273599]  [MGI Ref ID J:203372]

Ho A; Liu X; Sudhof TC. 2008. Deletion of Mint proteins decreases amyloid production in transgenic mouse models of Alzheimer's disease. J Neurosci 28(53):14392-400. [PubMed: 19118172]  [MGI Ref ID J:142874]

Hong S; Quintero-Monzon O; Ostaszewski BL; Podlisny DR; Cavanaugh WT; Yang T; Holtzman DM; Cirrito JR; Selkoe DJ. 2011. Dynamic Analysis of Amyloid beta-Protein in Behaving Mice Reveals Opposing Changes in ISF versus Parenchymal Abeta during Age-Related Plaque Formation. J Neurosci 31(44):15861-9. [PubMed: 22049429]  [MGI Ref ID J:177845]

Hook VY; Kindy M; Reinheckel T; Peters C; Hook G. 2009. Genetic cathepsin B deficiency reduces beta-amyloid in transgenic mice expressing human wild-type amyloid precursor protein. Biochem Biophys Res Commun 386(2):284-8. [PubMed: 19501042]  [MGI Ref ID J:151423]

Hosono-Fukao T; Ohtake-Niimi S; Hoshino H; Britschgi M; Akatsu H; Hossain MM; Nishitsuji K; van Kuppevelt TH; Kimata K; Michikawa M; Wyss-Coray T; Uchimura K. 2012. Heparan Sulfate Subdomains that are Degraded by Sulf Accumulate in Cerebral Amyloid ss Plaques of Alzheimer's Disease: Evidence from Mouse Models and Patients. Am J Pathol 180(5):2056-67. [PubMed: 22429964]  [MGI Ref ID J:183381]

Iascone DM; Padidam S; Pyfer MS; Zhang X; Zhao L; Chin J. 2013. Impairments in neurogenesis are not tightly linked to depressive behavior in a transgenic mouse model of Alzheimer's disease. PLoS One 8(11):e79651. [PubMed: 24244537]  [MGI Ref ID J:209698]

Kalinin S; Gavrilyuk V; Polak PE; Vasser R; Zhao J; Heneka MT; Feinstein DL. 2007. Noradrenaline deficiency in brain increases beta-amyloid plaque burden in an animal model of Alzheimer's disease. Neurobiol Aging 28(8):1206-14. [PubMed: 16837104]  [MGI Ref ID J:123899]

Kam TI; Song S; Gwon Y; Park H; Yan JJ; Im I; Choi JW; Choi TY; Kim J; Song DK; Takai T; Kim YC; Kim KS; Choi SY; Choi S; Klein WL; Yuan J; Jung YK. 2013. FcgammaRIIb mediates amyloid-beta neurotoxicity and memory impairment in Alzheimer's disease. J Clin Invest 123(7):2791-802. [PubMed: 23921129]  [MGI Ref ID J:201623]

Karl T; Bhatia S; Cheng D; Kim WS; Garner B. 2012. Cognitive phenotyping of amyloid precursor protein transgenic J20 mice. Behav Brain Res 228(2):392-7. [PubMed: 22197298]  [MGI Ref ID J:181714]

Kim WS; Li H; Ruberu K; Chan S; Elliott DA; Low JK; Cheng D; Karl T; Garner B. 2013. Deletion of Abca7 increases cerebral amyloid-beta accumulation in the J20 mouse model of Alzheimer's disease. J Neurosci 33(10):4387-94. [PubMed: 23467355]  [MGI Ref ID J:196282]

Kitaguchi H; Tomimoto H; Ihara M; Shibata M; Uemura K; Kalaria RN; Kihara T; Asada-Utsugi M; Kinoshita A; Takahashi R. 2009. Chronic cerebral hypoperfusion accelerates amyloid beta deposition in APPSwInd transgenic mice. Brain Res 1294:202-10. [PubMed: 19646974]  [MGI Ref ID J:157205]

Larson ME; Sherman MA; Greimel S; Kuskowski M; Schneider JA; Bennett DA; Lesne SE. 2012. Soluble alpha-Synuclein Is a Novel Modulator of Alzheimer's Disease Pathophysiology. J Neurosci 32(30):10253-66. [PubMed: 22836259]  [MGI Ref ID J:186543]

Lee JE; Han PL. 2013. An update of animal models of Alzheimer disease with a reevaluation of plaque depositions. Exp Neurobiol 22(2):84-95. [PubMed: 23833557]  [MGI Ref ID J:202532]

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Liu R; Lei JX; Luo C; Lan X; Chi L; Deng P; Lei S; Ghribi O; Liu QY. 2012. Increased EID1 nuclear translocation impairs synaptic plasticity and memory function associated with pathogenesis of Alzheimer's disease. Neurobiol Dis 45(3):902-12. [PubMed: 22186421]  [MGI Ref ID J:182043]

Lourenco FC; Galvan V; Fombonne J; Corset V; Llambi F; Muller U; Bredesen DE; Mehlen P. 2009. Netrin-1 interacts with amyloid precursor protein and regulates amyloid-beta production. Cell Death Differ 16(5):655-63. [PubMed: 19148186]  [MGI Ref ID J:164195]

Maesako M; Uemura K; Iwata A; Kubota M; Watanabe K; Uemura M; Noda Y; Asada-Utsugi M; Kihara T; Takahashi R; Shimohama S; Kinoshita A. 2013. Continuation of exercise is necessary to inhibit high fat diet-induced beta-amyloid deposition and memory deficit in amyloid precursor protein transgenic mice. PLoS One 8(9):e72796. [PubMed: 24023774]  [MGI Ref ID J:207565]

Maier M; Peng Y; Jiang L; Seabrook TJ; Carroll MC; Lemere CA. 2008. Complement C3 deficiency leads to accelerated amyloid beta plaque deposition and neurodegeneration and modulation of the microglia/macrophage phenotype in amyloid precursor protein transgenic mice. J Neurosci 28(25):6333-41. [PubMed: 18562603]  [MGI Ref ID J:135902]

Mairet-Coello G; Courchet J; Pieraut S; Courchet V; Maximov A; Polleux F. 2013. The CAMKK2-AMPK kinase pathway mediates the synaptotoxic effects of Abeta oligomers through Tau phosphorylation. Neuron 78(1):94-108. [PubMed: 23583109]  [MGI Ref ID J:197900]

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Meilandt WJ; Yu GQ; Chin J; Roberson ED; Palop JJ; Wu T; Scearce-Levie K; Mucke L. 2008. Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease. J Neurosci 28(19):5007-17. [PubMed: 18463254]  [MGI Ref ID J:135174]

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Moreno H; Wu WE; Lee T; Brickman A; Mayeux R; Brown TR; Small SA. 2007. Imaging the abeta-related neurotoxicity of Alzheimer disease. Arch Neurol 64(10):1467-77. [PubMed: 17923630]  [MGI Ref ID J:125332]

Mueller-Steiner S; Zhou Y; Arai H; Roberson ED; Sun B; Chen J; Wang X; Yu G; Esposito L; Mucke L; Gan L. 2006. Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's disease. Neuron 51(6):703-14. [PubMed: 16982417]  [MGI Ref ID J:113649]

Murakami K; Yokoyama S; Murata N; Ozawa Y; Irie K; Shirasawa T; Shimizu T. 2011. Insulin receptor mutation results in insulin resistance and hyperinsulinemia but does not exacerbate Alzheimer's-like phenotypes in mice. Biochem Biophys Res Commun 409(1):34-9. [PubMed: 21549686]  [MGI Ref ID J:172366]

Ongali B; Nicolakakis N; Lecrux C; Aboulkassim T; Rosa-Neto P; Papadopoulos P; Tong XK; Hamel E. 2010. Transgenic mice overexpressing APP and transforming growth factor-beta1 feature cognitive and vascular hallmarks of Alzheimer's disease. Am J Pathol 177(6):3071-80. [PubMed: 21088218]  [MGI Ref ID J:167619]

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Palop JJ; Chin J; Roberson ED; Wang J; Thwin MT; Bien-Ly N; Yoo J; Ho KO; Yu GQ; Kreitzer A; Finkbeiner S; Noebels JL; Mucke L. 2007. Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. Neuron 55(5):697-711. [PubMed: 17785178]  [MGI Ref ID J:126808]

Palop JJ; Jones B; Kekonius L; Chin J; Yu GQ; Raber J; Masliah E; Mucke L. 2003. Neuronal depletion of calcium-dependent proteins in the dentate gyrus is tightly linked to Alzheimer's disease-related cognitive deficits. Proc Natl Acad Sci U S A 100(16):9572-7. [PubMed: 12881482]  [MGI Ref ID J:106227]

Papadopoulos P; Rosa-Neto P; Rochford J; Hamel E. 2013. Pioglitazone improves reversal learning and exerts mixed cerebrovascular effects in a mouse model of Alzheimer's disease with combined amyloid-beta and cerebrovascular pathology. PLoS One 8(7):e68612. [PubMed: 23874687]  [MGI Ref ID J:204403]

Pickford F; Masliah E; Britschgi M; Lucin K; Narasimhan R; Jaeger PA; Small S; Spencer B; Rockenstein E; Levine B; Wyss-Coray T. 2008. The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice. J Clin Invest 118(6):2190-9. [PubMed: 18497889]  [MGI Ref ID J:137727]

Poirier R; Wolfer DP; Welzl H; Tracy J; Galsworthy MJ; Nitsch RM; Mohajeri MH. 2006. Neuronal neprilysin overexpression is associated with attenuation of Abeta-related spatial memory deficit. Neurobiol Dis 24(3):475-83. [PubMed: 17008108]  [MGI Ref ID J:147325]

Pozueta J; Lefort R; Shelanski ML. 2013. Synaptic changes in Alzheimer's disease and its models. Neuroscience 251:51-65. [PubMed: 22687952]  [MGI Ref ID J:207068]

Rama N; Goldschneider D; Corset V; Lambert J; Pays L; Mehlen P. 2012. Amyloid precursor protein regulates netrin-1-mediated commissural axon outgrowth. J Biol Chem 287(35):30014-23. [PubMed: 22782894]  [MGI Ref ID J:190417]

Roberson ED; Halabisky B; Yoo JW; Yao J; Chin J; Yan F; Wu T; Hamto P; Devidze N; Yu GQ; Palop JJ; Noebels JL; Mucke L. 2011. Amyloid-beta/Fyn-induced synaptic, network, and cognitive impairments depend on tau levels in multiple mouse models of Alzheimer's disease. J Neurosci 31(2):700-11. [PubMed: 21228179]  [MGI Ref ID J:168226]

Roberson ED; Scearce-Levie K; Palop JJ; Yan F; Cheng IH; Wu T; Gerstein H; Yu GQ; Mucke L. 2007. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model. Science 316(5825):750-4. [PubMed: 17478722]  [MGI Ref ID J:121330]

Sabbagh MN; Walker DG; Reid RT; Stadnick T; Anand K; Lue LF. 2008. Absence of effect of chronic nicotine administration on amyloid beta peptide levels in transgenic mice overexpressing mutated human APP (Sw, Ind). Neurosci Lett 448(2):217-20. [PubMed: 18926877]  [MGI Ref ID J:143592]

Sanchez PE; Zhu L; Verret L; Vossel KA; Orr AG; Cirrito JR; Devidze N; Ho K; Yu GQ; Palop JJ; Mucke L. 2012. Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model. Proc Natl Acad Sci U S A 109(42):E2895-903. [PubMed: 22869752]  [MGI Ref ID J:188597]

Sanchez-Mejia RO; Newman JW; Toh S; Yu GQ; Zhou Y; Halabisky B; Cisse M; Scearce-Levie K; Cheng IH; Gan L; Palop JJ; Bonventre JV; Mucke L. 2008. Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease. Nat Neurosci 11(11):1311-8. [PubMed: 18931664]  [MGI Ref ID J:141084]

Saura CA; Chen G; Malkani S; Choi SY; Takahashi RH; Zhang D; Gouras GK; Kirkwood A; Morris RG; Shen J. 2005. Conditional inactivation of presenilin 1 prevents amyloid accumulation and temporarily rescues contextual and spatial working memory impairments in amyloid precursor protein transgenic mice. J Neurosci 25(29):6755-64. [PubMed: 16033885]  [MGI Ref ID J:99847]

Seabrook TJ; Jiang L; Maier M; Lemere CA. 2006. Minocycline affects microglia activation, Abeta deposition, and behavior in APP-tg mice. Glia 53(7):776-82. [PubMed: 16534778]  [MGI Ref ID J:156129]

Sehgal N; Gupta A; Valli RK; Joshi SD; Mills JT; Hamel E; Khanna P; Jain SC; Thakur SS; Ravindranath V. 2012. Withania somnifera reverses Alzheimer's disease pathology by enhancing low-density lipoprotein receptor-related protein in liver. Proc Natl Acad Sci U S A 109(9):3510-5. [PubMed: 22308347]  [MGI Ref ID J:182629]

Serneels L; Van Biervliet J; Craessaerts K; Dejaegere T; Horre K; Van Houtvin T; Esselmann H; Paul S; Schafer MK; Berezovska O; Hyman BT; Sprangers B; Sciot R; Moons L; Jucker M; Yang Z; May PC; Karran E; Wiltfang J; D'Hooge R; De Strooper B. 2009. gamma-Secretase heterogeneity in the Aph1 subunit: relevance for Alzheimer's disease. Science 324(5927):639-42. [PubMed: 19299585]  [MGI Ref ID J:147990]

Simon AM; Schiapparelli L; Salazar-Colocho P; Cuadrado-Tejedor M; Escribano L; Lopez de Maturana R; Del Rio J; Perez-Mediavilla A; Frechilla D. 2009. Overexpression of wild-type human APP in mice causes cognitive deficits and pathological features unrelated to Abeta levels. Neurobiol Dis 33(3):369-78. [PubMed: 19101630]  [MGI Ref ID J:146301]

Sun B; Halabisky B; Zhou Y; Palop JJ; Yu G; Mucke L; Gan L. 2009. Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease. Cell Stem Cell 5(6):624-33. [PubMed: 19951690]  [MGI Ref ID J:155880]

Sun B; Zhou Y; Halabisky B; Lo I; Cho SH; Mueller-Steiner S; Devidze N; Wang X; Grubb A; Gan L. 2008. Cystatin C-cathepsin B axis regulates amyloid beta levels and associated neuronal deficits in an animal model of Alzheimer's disease. Neuron 60(2):247-57. [PubMed: 18957217]  [MGI Ref ID J:144067]

Takuma K; Fang F; Zhang W; Yan S; Fukuzaki E; Du H; Sosunov A; McKhann G; Funatsu Y; Nakamichi N; Nagai T; Mizoguchi H; Ibi D; Hori O; Ogawa S; Stern DM; Yamada K; Yan SS. 2009. RAGE-mediated signaling contributes to intraneuronal transport of amyloid-beta and neuronal dysfunction. Proc Natl Acad Sci U S A 106(47):20021-6. [PubMed: 19901339]  [MGI Ref ID J:154746]

Takuma K; Yao J; Huang J; Xu H; Chen X; Luddy J; Trillat AC; Stern DM; Arancio O; Yan SS. 2005. ABAD enhances Abeta-induced cell stress via mitochondrial dysfunction. FASEB J 19(6):597-8. [PubMed: 15665036]  [MGI Ref ID J:128890]

Talantova M; Sanz-Blasco S; Zhang X; Xia P; Akhtar MW; Okamoto S; Dziewczapolski G; Nakamura T; Cao G; Pratt AE; Kang YJ; Tu S; Molokanova E; McKercher SR; Hires SA; Sason H; Stouffer DG; Buczynski MW; Solomon JP; Michael S; Powers ET; Kelly JW; Roberts A; Tong G; Fang-Newmeyer T; Parker J; Holland EA; Zhang D; Nakanishi N; Chen HS; Wolosker H; Wang Y; Parsons LH; Ambasudhan R; Masliah E; Heinemann SF; Pina-Crespo JC; Lipton SA. 2013. Abeta induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss. Proc Natl Acad Sci U S A 110(27):E2518-27. [PubMed: 23776240]  [MGI Ref ID J:198709]

Tesseur I; Zou K; Esposito L; Bard F; Berber E; Can JV; Lin AH; Crews L; Tremblay P; Mathews P; Mucke L; Masliah E; Wyss-Coray T. 2006. Deficiency in neuronal TGF-beta signaling promotes neurodegeneration and Alzheimer's pathology. J Clin Invest 116(11):3060-9. [PubMed: 17080199]  [MGI Ref ID J:114572]

Thanopoulou K; Fragkouli A; Stylianopoulou F; Georgopoulos S. 2010. Scavenger receptor class B type I (SR-BI) regulates perivascular macrophages and modifies amyloid pathology in an Alzheimer mouse model. Proc Natl Acad Sci U S A 107(48):20816-21. [PubMed: 21076037]  [MGI Ref ID J:167168]

Tong XK; Nicolakakis N; Kocharyan A; Hamel E. 2005. Vascular remodeling versus amyloid beta-induced oxidative stress in the cerebrovascular dysfunctions associated with Alzheimer's disease. J Neurosci 25(48):11165-74. [PubMed: 16319316]  [MGI Ref ID J:202878]

Verret L; Mann EO; Hang GB; Barth AM; Cobos I; Ho K; Devidze N; Masliah E; Kreitzer AC; Mody I; Mucke L; Palop JJ. 2012. Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model. Cell 149(3):708-21. [PubMed: 22541439]  [MGI Ref ID J:186192]

Woo JA; Jung AR; Lakshmana MK; Bedrossian A; Lim Y; Bu JH; Park SA; Koo EH; Mook-Jung I; Kang DE. 2012. Pivotal role of the RanBP9-cofilin pathway in Abeta-induced apoptosis and neurodegeneration. Cell Death Differ 19(9):1413-23. [PubMed: 22361682]  [MGI Ref ID J:204630]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, hemizygous males are bred to wildtype siblings or to C57BL/6J inbred females. Pups born of carrier females have shown an increased mortality rate in our colonies. The Donating Researcher has observed an approximately 15% mortality rate in the first 6 months of life.
Mating SystemInbred x Hemizygote         (Female x Male)   28-OCT-13

Pricing and Purchasing

Supply Notes


Important Note

In March 2010, the donating investigator performed quantitative PCR on genomic DNA and determination of amyloid-beta levels in brain extract from the JAX Stock No. 006293 distribution colony (B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J also called "J20" line). Results of these analyses demonstrate that the current distribution colony maintains similar transgene copy number and expression as previously published (Mucke et. al. J Neurosci. 2000 Jun 1; 20(11): 4050-8).

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE only available to non-profit entities.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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