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| 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 B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
MMRRC Stock Number 034840. 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. | |||||||||||||||||||
- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
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Description
Strain Information
Former Names B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/J (Changed: 11-AUG-11 ) Type Mutant Stock; Transgenic; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Donating Investigator Robert Vassar, Northwestern University 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 (Abeta-42). 5XFAD mice generate Abeta-42 almost exclusively and rapidly accumulate massive cerebral levels. On the B6SJL F1 genetic 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 B6SJL hybrid background. 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 Abeta-42 induced neurodegeneration and amyloid plaque formation.
This strain is segregating heterozygous/wildtype for the retinal degeneration allele Pde6brd1.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. Of note, the APP transgene includes the 5' untranslated region and thus contains a putative interleukin-1beta translational enhancer element.
Related Strains
Alzheimer's Disease Models
View Alzheimer's Disease Models (108 strains)
008730 B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
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
- Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.
Alzheimer Disease 3
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. Acne Inversa, Familial, 3; ACNINV3 (PSEN1)
Cardiomyopathy, Dilated, 1u; CMD1U (PSEN1)
Frontotemporal Dementia; FTD (PSEN1)
Pick Disease of Brain (PSEN1)
assigned by genotype
Tg(APPSwFlLon,PSEN1*M146L*L286V)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 (MGI Ref ID J:112949)
- nervous system phenotype
- abnormal hippocampus morphology
- cortical layer 1 is significantly thinner than in control brains (MGI Ref ID J:112949)
- abnormal subiculum morphology
- neurons in subiculum are very pale, or absent (MGI Ref ID J:112949)
- abnormal neuron morphology
- some neurons contain intraneuronal aggregates and display disrupted morphology (MGI Ref ID J:112949)
- decreased cerebral cortex pyramidal cell number
- large neurons in cortical layer 5 are reduced in number (MGI Ref ID J:112949)
- amyloid beta deposits
- mice show Abeta42 deposits at 2 months of age; Abeta40 levels are lower in amyloid deposits; mice show robust intraneuronal amyloid deposition (MGI Ref ID J:112949)
- amyloid deposition increases rapidly with increasing age (MGI Ref ID J:112949)
- 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 (MGI Ref ID J:112949)
- brain inflammation
- transgenic mice display neuroinflammation (MGI Ref ID J:112949)
- 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 (MGI Ref ID J:112949)
- astrocytosis (MGI Ref ID J:112949)
- 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 (MGI Ref ID J:112949)
- immune system phenotype
- brain inflammation
- transgenic mice display neuroinflammation (MGI Ref ID J:112949)
- other phenotype
- amyloid beta deposits
- mice show Abeta42 deposits at 2 months of age; Abeta40 levels are lower in amyloid deposits; mice show robust intraneuronal amyloid deposition (MGI Ref ID J:112949)
- amyloid deposition increases rapidly with increasing age (MGI Ref ID J:112949)
- 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 (MGI Ref ID J:112949)
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
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas | ||
|---|---|---|---|
| Allele Name | transgene insertion 6799, Robert Vassar | ||
| Allele Type | Transgenic (random, expressed) | ||
| Common Name(s) | 5XFAD; 5XFAD APP/PS1; 5XFAD line Tg6799; Tg6799; | ||
| Mutation Made By | Robert Vassar, Northwestern University | ||
| Strain of Origin | (C57BL/6 x SJL)F1 | ||
| Expressed Gene | PSEN1, presenilin 1, human | ||
| Expressed Gene | APP695, amyloid beta (A4) precursor protein (chimeric), mouse/human chimera | ||
| Promoter | Thy1, thymus cell antigen 1, theta, mouse, laboratory | ||
| 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. | ||
| 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. [MGI Ref ID J:112949] [MGI Ref ID J:32213] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Generic Human PSEN1 cDNA Multiplex1, Melt Curve Analysis
Generic Pde6b, Standard PCR
Generic Tg(APP), Standard PCR
Tg(PSEN1), Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
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):10129-40. [PubMed: 17021169] [MGI Ref ID J:112949]
Additional References
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):3639-49. [PubMed: 17409228] [MGI Ref ID J:119403]
Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas relatedCai Y; Xue ZQ; Zhang XM; Li MB; Wang H; Luo XG; Cai H; Yan XX. 2012. An age-related axon terminal pathology around the first olfactory relay that involves amyloidogenic protein overexpression without plaque formation. Neuroscience 215:160-73. [PubMed: 22542680] [MGI Ref ID J:192436]
Carlo AS; Gustafsen C; Mastrobuoni G; Nielsen MS; Burgert T; Hartl D; Rohe M; Nykjaer A; Herz J; Heeren J; Kempa S; Petersen CM; Willnow TE. 2013. The pro-neurotrophin receptor sortilin is a major neuronal apolipoprotein E receptor for catabolism of amyloid-beta peptide in the brain. J Neurosci 33(1):358-70. [PubMed: 23283348] [MGI Ref ID J:193915]
Christensen DZ; Bayer TA; Wirths O. 2009. Formic acid is essential for immunohistochemical detection of aggregated intraneuronal Abeta peptides in mouse models of Alzheimer's disease. Brain Res 1301:116-25. [PubMed: 19751708] [MGI Ref ID J:158791]
Cortes-Canteli M; Paul J; Norris EH; Bronstein R; Ahn HJ; Zamolodchikov D; Bhuvanendran S; Fenz KM; Strickland S. 2010. Fibrinogen and beta-amyloid association alters thrombosis and fibrinolysis: a possible contributing factor to Alzheimer's disease. Neuron 66(5):695-709. [PubMed: 20547128] [MGI Ref ID J:167873]
Cui Y; Huang M; He Y; Zhang S; Luo Y. 2011. Genetic Ablation of Apolipoprotein A-IV Accelerates Alzheimer's Disease Pathogenesis in a Mouse Model. Am J Pathol 178(3):1298-308. [PubMed: 21356380] [MGI Ref ID J:169682]
Devi L; Ohno M. 2010. Genetic reductions of beta-site amyloid precursor protein-cleaving enzyme 1 and amyloid-beta ameliorate impairment of conditioned taste aversion memory in 5XFAD Alzheimer's disease model mice. Eur J Neurosci 31(1):110-8. [PubMed: 20092558] [MGI Ref ID J:158363]
Devi L; Ohno M. 2012. Mitochondrial dysfunction and accumulation of the beta-secretase-cleaved C-terminal fragment of APP in Alzheimer's disease transgenic mice. Neurobiol Dis 45(1):417-24. [PubMed: 21933711] [MGI Ref ID J:179837]
Devi L; Ohno M. 2010. Phospho-eIF2alpha level is important for determining abilities of BACE1 reduction to rescue cholinergic neurodegeneration and memory defects in 5XFAD mice. PLoS One 5(9):e12974. [PubMed: 20886088] [MGI Ref ID J:165103]
Graff J; Rei D; Guan JS; Wang WY; Seo J; Hennig KM; Nieland TJ; Fass DM; Kao PF; Kahn M; Su SC; Samiei A; Joseph N; Haggarty SJ; Delalle I; Tsai LH. 2012. An epigenetic blockade of cognitive functions in the neurodegenerating brain. Nature 483(7388):222-6. [PubMed: 22388814] [MGI Ref ID J:181683]
Hillmann A; Hahn S; Schilling S; Hoffmann T; Demuth HU; Bulic B; Schneider-Axmann T; Bayer TA; Weggen S; Wirths O. 2012. No improvement after chronic ibuprofen treatment in the 5XFAD mouse model of Alzheimer's disease. Neurobiol Aging 33(4):833.e39-50. [PubMed: 21943956] [MGI Ref ID J:188189]
Jawhar S; Trawicka A; Jenneckens C; Bayer TA; Wirths O. 2012. Motor deficits, neuron loss, and reduced anxiety coinciding with axonal degeneration and intraneuronal Abeta aggregation in the 5XFAD mouse model of Alzheimer's disease. Neurobiol Aging 33(1):196.e29-40. [PubMed: 20619937] [MGI Ref ID J:188235]
Jawhar S; Wirths O; Schilling S; Graubner S; Demuth HU; Bayer TA. 2011. Overexpression of glutaminyl cyclase, the enzyme responsible for pyroglutamate A{beta} formation, induces behavioral deficits, and glutaminyl cyclase knock-out rescues the behavioral phenotype in 5XFAD mice. J Biol Chem 286(6):4454-60. [PubMed: 21148560] [MGI Ref ID J:169481]
Kalinin S; Polak PE; Lin SX; Sakharkar AJ; Pandey SC; Feinstein DL. 2012. The noradrenaline precursor L-DOPS reduces pathology in a mouse model of Alzheimer's disease. Neurobiol Aging 33(8):1651-63. [PubMed: 21705113] [MGI Ref ID J:188202]
Kim C; Nam DW; Park SY; Song H; Hong HS; Boo JH; Jung ES; Kim Y; Baek JY; Kim KS; Cho JW; Mook-Jung I. 2013. O-linked beta-N-acetylglucosaminidase inhibitor attenuates beta-amyloid plaque and rescues memory impairment. Neurobiol Aging 34(1):275-85. [PubMed: 22503002] [MGI Ref ID J:191369]
Kimura R; Devi L; Ohno M. 2010. Partial reduction of BACE1 improves synaptic plasticity, recent and remote memories in Alzheimer's disease transgenic mice. J Neurochem 113(1):248-61. [PubMed: 20089133] [MGI Ref ID J:174832]
Kimura R; Ohno M. 2009. Impairments in remote memory stabilization precede hippocampal synaptic and cognitive failures in 5XFAD Alzheimer mouse model. Neurobiol Dis 33(2):229-35. [PubMed: 19026746] [MGI Ref ID J:144743]
Kook SY; Hong HS; Moon M; Ha CM; Chang S; Mook-Jung I. 2012. Abeta1-42-RAGE Interaction Disrupts Tight Junctions of the Blood-Brain Barrier Via Ca2+-Calcineurin Signaling. J Neurosci 32(26):8845-54. [PubMed: 22745485] [MGI Ref ID J:185647]
Leroy K; Ando K; Laporte V; Dedecker R; Suain V; Authelet M; Heraud C; Pierrot N; Yilmaz Z; Octave JN; Brion JP. 2012. Lack of tau proteins rescues neuronal cell death and decreases amyloidogenic processing of APP in APP/PS1 mice. Am J Pathol 181(6):1928-40. [PubMed: 23026200] [MGI Ref ID J:190305]
Mijatovic J; Piltonen M; Alberton P; Mannisto PT; Saarma M; Piepponen TP. 2011. Constitutive Ret signaling is protective for dopaminergic cell bodies but not for axonal terminals. Neurobiol Aging 32(8):1486-94. [PubMed: 19767128] [MGI Ref ID J:176716]
Moechars D; Lorent K; De Strooper B; Dewachter I; Van Leuven F. 1996. Expression in brain of amyloid precursor protein mutated in the alpha-secretase site causes disturbed behavior, neuronal degeneration and premature death in transgenic mice. EMBO J 15(6):1265-74. [PubMed: 8635459] [MGI Ref ID J:32213]
Ohno M. 2009. Failures to reconsolidate memory in a mouse model of Alzheimer's disease. Neurobiol Learn Mem 92(3):455-9. [PubMed: 19435612] [MGI Ref ID J:154421]
Ohno M; Cole SL; Yasvoina M; Zhao J; Citron M; Berry R; Disterhoft JF; Vassar R. 2007. BACE1 gene deletion prevents neuron loss and memory deficits in 5XFAD APP/PS1 transgenic mice. Neurobiol Dis 26(1):134-45. [PubMed: 17258906] [MGI Ref ID J:119002]
Sadleir KR; Vassar R. 2012. Cdk5 protein inhibition and Abeta42 increase BACE1 protein level in primary neurons by a post-transcriptional mechanism: implications of CDK5 as a therapeutic target for Alzheimer disease. J Biol Chem 287(10):7224-35. [PubMed: 22223639] [MGI Ref ID J:182773]
Wirths O; Erck C; Martens H; Harmeier A; Geumann C; Jawhar S; Kumar S; Multhaup G; Walter J; Ingelsson M; Degerman-Gunnarsson M; Kalimo H; Huitinga I; Lannfelt L; Bayer TA. 2010. Identification of low molecular weight pyroglutamate A{beta} oligomers in Alzheimer disease: a novel tool for therapy and diagnosis. J Biol Chem 285(53):41517-24. [PubMed: 20971852] [MGI Ref ID J:167567]
Wittnam JL; Portelius E; Zetterberg H; Gustavsson MK; Schilling S; Koch B; Demuth HU; Blennow K; Wirths O; Bayer TA. 2012. Pyroglutamate amyloid beta (Abeta) aggravates behavioral deficits in transgenic amyloid mouse model for Alzheimer disease. J Biol Chem 287(11):8154-62. [PubMed: 22267726] [MGI Ref ID J:182761]
Woo DC; Lee SH; Lee DW; Kim SY; Kim GY; Rhim HS; Choi CB; Kim HY; Lee CU; Choe BY. 2010. Regional metabolic alteration of Alzheimer's disease in mouse brain expressing mutant human APP-PS1 by 1H HR-MAS. Behav Brain Res 211(1):125-31. [PubMed: 20307581] [MGI Ref ID J:159678]
You H; Tsutsui S; Hameed S; Kannanayakal TJ; Chen L; Xia P; Engbers JD; Lipton SA; Stys PK; Zamponi GW. 2012. Abeta neurotoxicity depends on interactions between copper ions, prion protein, and N-methyl-D-aspartate receptors. Proc Natl Acad Sci U S A 109(5):1737-42. [PubMed: 22307640] [MGI Ref ID J:182028]
Youmans KL; Tai LM; Nwabuisi-Heath E; Jungbauer L; Kanekiyo T; Gan M; Kim J; Eimer WA; Estus S; Rebeck GW; Weeber EJ; Bu G; Yu C; Ladu MJ. 2012. APOE4-specific changes in Abeta accumulation in a new transgenic mouse model of Alzheimer disease. J Biol Chem 287(50):41774-86. [PubMed: 23060451] [MGI Ref ID J:193422]
Yun SM; Cho SJ; Song JC; Song SY; Jo SA; Jo C; Yoon K; Tanzi RE; Choi EJ; Koh YH. 2013. SUMO1 modulates Abeta generation via BACE1 accumulation. Neurobiol Aging 34(3):650-62. [PubMed: 22975420] [MGI Ref ID J:194511]
Zhang XM; Cai Y; Xiong K; Cai H; Luo XG; Feng JC; Clough RW; Struble RG; Patrylo PR; Yan XX. 2009. Beta-secretase-1 elevation in transgenic mouse models of Alzheimer's disease is associated with synaptic/axonal pathology and amyloidogenesis: implications for neuritic plaque development. Eur J Neurosci 30(12):2271-83. [PubMed: 20092570] [MGI Ref ID J:157228]
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):3639-49. [PubMed: 17409228] [MGI Ref ID J:119403]
Health & husbandry
Health & Colony Maintenance Information
Colony Maintenance
Breeding & Husbandry When maintaining a live colony, hemizygous mice may be bred to B6SJLF1/J (Stock No. 100012). Diet Information LabDiet® 5K52/5K67
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
This strain is currently Transferred.
General Supply Notes
- Genomic DNA is available for this strain from the Mouse DNA Resource.
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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.Ordering Information
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