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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 B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
MMRRC Stock Number 034829. 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. | |||||||||||||||||||
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- Disease & phenotype
- Genes & alleles
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Description
Strain Information
Former Names B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J (Changed: 10-AUG-11 ) B6C3-Tg(APPswe, PSEN1dE9)85Dbo/J (Changed: 01-FEB-06 ) B6C3-Tg(APP695)85Dbo Tg(PSEN1)85Dbo (Changed: 15-DEC-04 ) B6C3-Tg(APP695)85Dbo Tg(PSEN1)85Dbo/J (Changed: 15-DEC-04 ) Mo/Hu APPswe PS1dE9 (Changed: 15-DEC-04 ) Type Mutant Strain; Transgenic; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Donating Investigator Dr. David R. Borchelt, McKnight Brain Inst, Univ of Florida Description
Double transgenic mice express a chimeric mouse/human amyloid precursor protein (Mo/HuAPP695swe) and a mutant human presenilin 1 (PS1-dE9) both directed to CNS neurons. Both mutations are associated with early-onset Alzheimer's disease. The "humanized" Mo/HuAPP695swe transgene allows the mice to secrete a human A-beta peptide. Both the transgenic peptide and holoprotein can be detected by antibodies specific for human sequence within this region (Signet Laboratories' monoclonal 6E10 antibody). The included Swedish mutations (K595N/M596L) elevate the amount of A-beta produced from the transgene by favoring processing through the beta-secretase pathway. This "humanized" Mo/HuAPP695swe protein is immunodetected in whole brain protein homogenates. The transgenic mutant human presenilin protein (PS1-dE9), which in high levels displaces detectable endogenous mouse protein, is also immunodetected in whole brain protein homogenates. The donating investigator reports that transgenic mice develop beta-amyloid deposits in brain by six to seven months of age. These animals also display a slight alteration in their tail phenotype that is believed to be due to the mixed genetic background of the strain and is not related to transgene expression. Hemizygous mice on the C57BL/6 background (N9B6) exhibit a high incidence of seizures, as detected by video-EEG. 25% of transgenic mice, 3 to 3.5 months in age, exhibit at least 1 seizure. By 4.5 months of age, seizure incidence increases to 55%. 10-15% mortality is reported for transgenic mice on the congenic (N9) C57BL/6 background (Minkeviciene et al. J Neurosci. 2009). Hemizygous mice, on the congenic C57BL/6J background (N13), 17-18 weeks in age, exhibit epileptiform discharges as detected by video-EEG. Mortality was 38% (6/16) and some mutant mice experienced spontaneous seizures during the experiments. Antiepileptic drugs (carbamazepine, phenytoin, valproate) reduce the frequency of spontaneous electrographic epileptiform discharges (Ziyatdinova et al. Epilepsy Res 2011). These mice may be useful in studies of neurological disorders of the brain, specifically Alzheimer's disease, amyloid plaque formation, and aging.This strain does not carry the retinal degeneration allele Pde6brd1.
Development
Two expression plasmids (Mo/HuAPP695swe and PS1-dE9) were designed to each be controlled by independent mouse prion protein (PrP) promoter elements, directing transgene expression predominantly to CNS neurons. The Mo/HuAPP695swe transgene expresses a “humanized” mouse amyloid beta (A4) precursor protein gene modified at three amino acids to reflect the human residues and further modified to contain the K595N/M596L mutations linked to familial Alzheimers. The PS1-dE9 transgene expresses a mutant human presenilin 1 carrying the exon-9-deleted variant (PSEN1dE9) associated with familial Alzheimer's disease. These constructs were coinjected into B6C3HF2 pronuclei and insertion of the transgenes occured at a single locus. Founder line 85 was obtained and the resulting colony was maintained as a hemizygote by crossing transgenic mice to B6C3F1/J mice.
Related Strains
Alzheimer's Disease Models
View Alzheimer's Disease Models (107 strains)
005864 B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
005866 B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/Mmjax 003378 B6C3-Tg(APP695)3Dbo Tg(PSEN1)5Dbo/J 003627 B6C3-Tg(HD82Gln)81Dbo/J 003375 C3B6-Tg(APP695)3Dbo/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)
Cerebral Amyloid Angiopathy, App-Related (APP)
Frontotemporal Dementia; FTD (PSEN1)
Pick Disease of Brain (PSEN1)
assigned by genotype
Tg(APPswe,PSEN1dE9)85Dbo/0
involves: C3H/HeJ * C57BL/6J
- nervous system phenotype
- amyloid beta deposits
- plaques are abundant in hippocampus and cortex by 9 months of age (MGI Ref ID J:87691)
- occasional deposits can be found in mice as young as 6 months of age (MGI Ref ID J:87691)
- ratio of amyloid beta peptide 40:42 is 0.50:1 (MGI Ref ID J:87691)
- deposits observed in hippocampus by 6 months of age (MGI Ref ID J:139071)
- reduced long term potentiation
- transient long term potentiation (t-LTP) is reduced in transgenics and is age-independent (MGI Ref ID J:139071)
- other phenotype
- amyloid beta deposits
- plaques are abundant in hippocampus and cortex by 9 months of age (MGI Ref ID J:87691)
- occasional deposits can be found in mice as young as 6 months of age (MGI Ref ID J:87691)
- ratio of amyloid beta peptide 40:42 is 0.50:1 (MGI Ref ID J:87691)
- deposits observed in hippocampus by 6 months of age (MGI Ref ID J:139071)
- behavior/neurological phenotype
- abnormal spatial reference memory
- transgenic mice exhibit a 4-5% higher preference for the arm of the radial arm water maze that held the platform on the previous day (MGI Ref ID J:139071)
- 13 month old transgenic mice commit more errors in the water maze than controls, at 7 months of age both groups test similarly (MGI Ref ID J:139071)
- impaired coordination
- 14 month old transgenic mice exhibit a reduced ability to maintain balance on a rotarod (MGI Ref ID J:139071)
- growth/size phenotype
- decreased body weight
- at 14 months, transgenics weigh less than controls (MGI Ref ID J:139071)
Tg(APPswe,PSEN1dE9)85Dbo/0
B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
- nervous system phenotype
- amyloid beta deposits
- sparse deposits observed at 21 weeks of age, however, numerous deposits are observed at 45 and 60 weeks (MGI Ref ID J:113199)
- deposits are more extensive in females (MGI Ref ID J:113199)
- level of brain amyloid beta peptide 42 is predominant over 40; levels increase dramatically after 20 weeks of age (MGI Ref ID J:113199)
- senile plaques detected by thioflavin S or the anti-amyloid beta antibody, 3D6, as early as 4 months of age (MGI Ref ID J:113200)
- plaques are restricted to cortex and hippocampus at time points up to 12 months of age (MGI Ref ID J:113200)
- plaques increase in number and size over time (MGI Ref ID J:113200)
- exhibits an overall increase in soluble and insoluble amyloid beta peptide 40 and 42 between 4 and 12 months (MGI Ref ID J:113200)
- insoluble amyloid beta42 is increased 2-fold in cerebrum of sucrose-fed mice as compared to water-fed control (MGI Ref ID J:129021)
- total amyloid beta levels are increased by 3.6 fold in sucrose fed mice (MGI Ref ID J:129021)
- amyloid beta deposition is increased by 2.9-fold as determined by immunohistochemical and morphometric analysis in sucrose-fed mice (MGI Ref ID J:129021)
- cerebral amyloid angiopathy
- behavior/neurological phenotype
- abnormal spatial learning
- transgenic mice fed sucrose water failed to learn Morris water maze test after 5 days of training (MGI Ref ID J:129021)
- water-fed transgenic mice retained some learning ability over 5 day test period, but did not perform as well in the water maze test as non-transgenic controls (MGI Ref ID J:129021)
- increased fluid intake
- mice fed sucrose water exhibited increased water consumption (MGI Ref ID J:129021)
- homeostasis/metabolism phenotype
- impaired glucose tolerance
- mice fed sucrose water displayed an impaired glucose tolerance as compared to water-fed control (MGI Ref ID J:129021)
- increased circulating cholesterol level
- total cholesterol, but not HDL, levels are increased 30% in mice fed sucrose water as compared to water-fed control (MGI Ref ID J:129021)
- increased circulating insulin level
- fasting plasma insulin levels are increased 3 fold in mice fed sucrose water as compared to water-fed control (MGI Ref ID J:129021)
- increased circulating triglyceride level
- elevated plasma triglyceride levels observed in females at 15 weeks of age (MGI Ref ID J:113199)
- cardiovascular system phenotype
- vasculature congestion (MGI Ref ID J:113200)
- other phenotype
- amyloidosis (MGI Ref ID J:129021)
- amyloid beta deposits
- sparse deposits observed at 21 weeks of age, however, numerous deposits are observed at 45 and 60 weeks (MGI Ref ID J:113199)
- deposits are more extensive in females (MGI Ref ID J:113199)
- level of brain amyloid beta peptide 42 is predominant over 40; levels increase dramatically after 20 weeks of age (MGI Ref ID J:113199)
- senile plaques detected by thioflavin S or the anti-amyloid beta antibody, 3D6, as early as 4 months of age (MGI Ref ID J:113200)
- plaques are restricted to cortex and hippocampus at time points up to 12 months of age (MGI Ref ID J:113200)
- plaques increase in number and size over time (MGI Ref ID J:113200)
- exhibits an overall increase in soluble and insoluble amyloid beta peptide 40 and 42 between 4 and 12 months (MGI Ref ID J:113200)
- insoluble amyloid beta42 is increased 2-fold in cerebrum of sucrose-fed mice as compared to water-fed control (MGI Ref ID J:129021)
- total amyloid beta levels are increased by 3.6 fold in sucrose fed mice (MGI Ref ID J:129021)
- amyloid beta deposition is increased by 2.9-fold as determined by immunohistochemical and morphometric analysis in sucrose-fed mice (MGI Ref ID J:129021)
- cerebral amyloid angiopathy
- growth/size phenotype
- increased body weight
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Tg(APPswe,PSEN1dE9)85Dbo/0
involves: C3H * C57BL/6
- nervous system phenotype
- *normal* nervous system phenotype
- striatal volume is similar in both transgenic and wild-type at either 6 or 12 months of age (MGI Ref ID J:145530)
- abnormal medium spiny neuron morphology
- nuclei of medium spiny stellate neurons in both 6 and 12 month old transgenics are smaller and darker than wild-type (MGI Ref ID J:145530)
- decreased neuron number
- numbers of neurons are reduced in striatum of 12, but not 6, month old transgenics (MGI Ref ID J:145530)
- neuron degeneration
- other phenotype
- amyloidosis
- increase in circulating amyloid beta protein levels (MGI Ref ID J:186924)
- homeostasis/metabolism phenotype
- *normal* homeostasis/metabolism phenotype
- mutants exhibit normal body weight, blood glucose, plasma insulin levels, nonfasting blood glucose and nonfasting plasma insulin, and normal glucose and insulin tolerance, indicating normal glucose homeostasis and insulin sensitivity (MGI Ref ID J:186924)
Tg(APPswe,PSEN1dE9)85Dbo/0
B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
- mortality/aging
- premature death
- about 40% of mice are lost by 12 months of age (MGI Ref ID J:160557)
- behavior/neurological phenotype
- abnormal spatial learning
- 6 month old mutants exhibit slower visuospatial learning than control mice (MGI Ref ID J:172426)
- in the visuospatial re-learning test performed at 9, 11, 13, 15, and 18 months of age, mutants exhibit a decrease in the speed of re-learning the task compared to controls (MGI Ref ID J:172426)
- severely impaired performance in a morris water maze with much longer latencies to reach a hidden platform (MGI Ref ID J:160557)
- performance in a morris water maze declines between 3 and 12 months of age (MGI Ref ID J:160557)
- impaired passive avoidance behavior (MGI Ref ID J:160557)
- nervous system phenotype
- amyloid beta deposits (MGI Ref ID J:160557)
- astrocytosis (MGI Ref ID J:160557)
- axon degeneration
- axon degeneration and synapse loss (MGI Ref ID J:160557)
- other phenotype
- amyloid beta deposits (MGI Ref ID J:160557)
- taste/olfaction phenotype
- *normal* taste/olfaction phenotype
- mutants do not exhibit Alzheimer's disease-related impairments in olfactory performance in tests based on an operant conditioning procedure and in tests based on a habituation/dishabituation procedure (MGI Ref ID J:172426)
This mouse can be used to support research in many areas including:
APP relatedNeurobiology Research
Alzheimer's Disease
APP and PSEN1 mutants
Presenilin mutants
strains expressing mutant APP
Behavioral and Learning Defects
Epilepsy
electroconvulsive seizures
Neurodegeneration
Tg(APPswe,PSEN1dE9)85Dbo relatedNeurobiology Research
Neurodegeneration
Neurobiology Research
Alzheimer's Disease
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Tg(APPswe,PSEN1dE9)85Dbo | ||
|---|---|---|---|
| Allele Name | transgene insertion 85, David R Borchelt | ||
| Allele Type | Transgenic (random, expressed) | ||
| Common Name(s) | APP/PS1; APPswe/PS1dE9; APPswe/PS1deltaE9; APdE9; Mo/Hu APPswe PS1dE9; | ||
| Mutation Made By | Dr. David Borchelt, McKnight Brain Inst, Univ of Florida | ||
| Strain of Origin | (C57BL/6 x C3H)F2 | ||
| Expressed Gene | APP, amyloid beta (A4) precursor protein, human | ||
| Expressed Gene | PSEN1, presenilin 1, human | ||
| Promoter | Prn, prion protein gene complex, mouse, laboratory | ||
| General Note | Mice carrying this double transgene develop beta-amyloid deposits in the brain by 6 to 7 months of age. | ||
| Molecular Note | Two transgenes inserted at a single locus. Each transgene is controlled by the mouse prion promoter and contains a cDNA sequence. In one transgene the cDNA encodes a chimeric amyloid beta (A4) precursor protein (APPswe). In the second transgene the cDNA encodes the "DeltaE9" mutation of human presenilin 1. The DeltaE9 mutation of the human presenilin 1 gene is a deletion of exon 9 and corresponds to a form of early-onset Alzheimer's disease. The amyloid beta precursor protein coding sequences were altered by replacing mouse sequence encoding three amino acids of the A-beta domain with the human coding sequence for these residues. The chimeric amyloid beta (A4) precursor protein sequence was then further modified to encode the Swedish mutations K595N/M596L found in human. Both the transgenic peptide and holoprotein are detected by Signet Laboratories' monoclonal 6E10 antibody, which is specific for human sequence within this region. Human presenilin protein, which in high levels displaces detectable endogenous mouse protein, is immunodetected in the double transgenic mouse in whole brain protein homogenates. Human amyloid precursor protein is also immunodetected in these mice in whole brain protein homogenates. [MGI Ref ID J:78664] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Generic Mouse App cDNA, Melt Curve Analysis
Generic Tg(APP), Standard PCR
Tg(PSEN1), Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Jankowsky JL; Fadale DJ; Anderson J; Xu GM; Gonzales V; Jenkins NA; Copeland NG; Lee MK; Younkin LH; Wagner SL; Younkin SG; Borchelt DR. 2004. Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase. Hum Mol Genet 13(2):159-70. [PubMed: 14645205] [MGI Ref ID J:87691]
Jankowsky JL; Slunt HH; Ratovitski T; Jenkins NA; Copeland NG; Borchelt DR. 2001. Co-expression of multiple transgenes in mouse CNS: a comparison of strategies. Biomol Eng 17(6):157-65. [PubMed: 11337275] [MGI Ref ID J:78664]
Reiserer RS; Harrison FE; Syverud DC; McDonald MP. 2007. Impaired spatial learning in the APP + PSEN1DeltaE9 bigenic mouse model of Alzheimer's disease. Genes Brain Behav 6(1):54-65. [PubMed: 17233641] [MGI Ref ID J:116798]
Additional References
Fukui H; Diaz F; Garcia S; Moraes CT. 2007. Cytochrome c oxidase deficiency in neurons decreases both oxidative stress and amyloid formation in a mouse model of Alzheimer's disease Proc Natl Acad Sci U S A 104(35):14163-8. [PubMed: 17715058] [MGI Ref ID J:123812]
Sood A; Warren Beach J; Webster SJ; Terry AV; Buccafusco JJ. 2007. The effects of JWB1-84-1 on memory-related task performance by amyloid Abeta transgenic mice and by young and aged monkeys. Neuropharmacology 53(5):588-600. [PubMed: 17698153] [MGI Ref ID J:124366]
Tg(APPswe,PSEN1dE9)85Dbo relatedBakalash S; Pham M; Koronyo Y; Salumbides BC; Kramerov A; Seidenberg H; Berel D; Black KL; Koronyo-Hamaoui M. 2011. Egr1 expression is induced following glatiramer acetate immunotherapy in rodent models of glaucoma and Alzheimer's disease. Invest Ophthalmol Vis Sci 52(12):9033-46. [PubMed: 21969301] [MGI Ref ID J:189462]
Bernardo A; Harrison FE; McCord M; Zhao J; Bruchey A; Davies SS; Jackson Roberts L 2nd; Mathews PM; Matsuoka Y; Ariga T; Yu RK; Thompson R; McDonald MP. 2009. Elimination of GD3 synthase improves memory and reduces amyloid-beta plaque load in transgenic mice. Neurobiol Aging 30(11):1777-91. [PubMed: 18258340] [MGI Ref ID J:152957]
Bero AW; Yan P; Roh JH; Cirrito JR; Stewart FR; Raichle ME; Lee JM; Holtzman DM. 2011. Neuronal activity regulates the regional vulnerability to amyloid-beta deposition. Nat Neurosci 14(6):750-6. [PubMed: 21532579] [MGI Ref ID J:173925]
Burdo JR; Chen Q; Calcutt NA; Schubert D. 2009. The pathological interaction between diabetes and presymptomatic Alzheimer's disease. Neurobiol Aging 30(12):1910-7. [PubMed: 18372080] [MGI Ref ID J:155161]
Burgess BL; McIsaac SA; Naus KE; Chan JY; Tansley GH; Yang J; Miao F; Ross CJ; van Eck M; Hayden MR; van Nostrand W; St George-Hyslop P; Westaway D; Wellington CL. 2006. Elevated plasma triglyceride levels precede amyloid deposition in Alzheimer's disease mouse models with abundant A beta in plasma. Neurobiol Dis 24(1):114-27. [PubMed: 16899370] [MGI Ref ID J:113199]
Butler D; Hwang J; Estick C; Nishiyama A; Kumar SS; Baveghems C; Young-Oxendine HB; Wisniewski ML; Charalambides A; Bahr BA. 2011. Protective effects of positive lysosomal modulation in Alzheimer's disease transgenic mouse models. PLoS One 6(6):e20501. [PubMed: 21695208] [MGI Ref ID J:174789]
Butovsky O; Kunis G; Koronyo-Hamaoui M; Schwartz M. 2007. Selective ablation of bone marrow-derived dendritic cells increases amyloid plaques in a mouse Alzheimer's disease model. Eur J Neurosci 26(2):413-6. [PubMed: 17623022] [MGI Ref ID J:127277]
Cao D; Lu H; Lewis TL; Li L. 2007. Intake of sucrose-sweetened water induces insulin resistance and exacerbates memory deficits and amyloidosis in a transgenic mouse model of Alzheimer disease. J Biol Chem 282(50):36275-82. [PubMed: 17942401] [MGI Ref ID J:129021]
Chen L; Choi JJ; Choi YJ; Hennig B; Toborek M. 2012. HIV-1 Tat-induced cerebrovascular toxicity is enhanced in mice with amyloid deposits. Neurobiol Aging 33(8):1579-90. [PubMed: 21764480] [MGI Ref ID J:188199]
Chen SQ; Cai Q; Shen YY; Wang PJ; Teng GJ; Zhang W; Zang FC. 2012. Age-related changes in brain metabolites and cognitive function in APP/PS1 transgenic mice. Behav Brain Res 235(1):1-6. [PubMed: 22828014] [MGI Ref ID J:193519]
Cherry JD; Liu B; Frost JL; Lemere CA; Williams JP; Olschowka JA; O'Banion MK. 2012. Galactic cosmic radiation leads to cognitive impairment and increased abeta plaque accumulation in a mouse model of Alzheimer's disease. PLoS One 7(12):e53275. [PubMed: 23300905] [MGI Ref ID J:195722]
Choi SH; Leight SN; Lee VM; Li T; Wong PC; Johnson JA; Saraiva MJ; Sisodia SS. 2007. Accelerated Abeta deposition in APPswe/PS1deltaE9 mice with hemizygous deletions of TTR (transthyretin). J Neurosci 27(26):7006-10. [PubMed: 17596449] [MGI Ref ID J:122976]
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]
Cohen E; Paulsson JF; Blinder P; Burstyn-Cohen T; Du D; Estepa G; Adame A; Pham HM; Holzenberger M; Kelly JW; Masliah E; Dillin A. 2009. Reduced IGF-1 signaling delays age-associated proteotoxicity in mice. Cell 139(6):1157-69. [PubMed: 20005808] [MGI Ref ID J:157007]
Cramer PE; Cirrito JR; Wesson DW; Lee CY; Karlo JC; Zinn AE; Casali BT; Restivo JL; Goebel WD; James MJ; Brunden KR; Wilson DA; Landreth GE. 2012. ApoE-directed therapeutics rapidly clear beta-amyloid and reverse deficits in AD mouse models. Science 335(6075):1503-6. [PubMed: 22323736] [MGI Ref ID J:181688]
Crouch PJ; Hung LW; Adlard PA; Cortes M; Lal V; Filiz G; Perez KA; Nurjono M; Caragounis A; Du T; Laughton K; Volitakis I; Bush AI; Li QX; Masters CL; Cappai R; Cherny RA; Donnelly PS; White AR; Barnham KJ. 2009. Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation. Proc Natl Acad Sci U S A 106(2):381-6. [PubMed: 19122148] [MGI Ref ID J:143873]
Cui W; Sun Y; Wang Z; Xu C; Peng Y; Li R. 2012. Liver X receptor activation attenuates inflammatory response and protects cholinergic neurons in APP/PS1 transgenic mice. Neuroscience 210:200-10. [PubMed: 22425753] [MGI Ref ID J:184718]
D'Amico M; Di Filippo C; Marfella R; Abbatecola AM; Ferraraccio F; Rossi F; Paolisso G. 2010. Long-term inhibition of dipeptidyl peptidase-4 in Alzheimer's prone mice. Exp Gerontol 45(3):202-7. [PubMed: 20005285] [MGI Ref ID J:158446]
Ding Y; Qiao A; Wang Z; Goodwin JS; Lee ES; Block ML; Allsbrook M; McDonald MP; Fan GH. 2008. Retinoic acid attenuates beta-amyloid deposition and rescues memory deficits in an Alzheimer's disease transgenic mouse model. J Neurosci 28(45):11622-34. [PubMed: 18987198] [MGI Ref ID J:143199]
Donmez G; Wang D; Cohen DE; Guarente L. 2010. SIRT1 suppresses beta-amyloid production by activating the alpha-secretase gene ADAM10. Cell 142(2):320-32. [PubMed: 20655472] [MGI Ref ID J:163978]
Du J; Sun B; Chen K; Fan L; Wang Z. 2009. Antagonist of peroxisome proliferator-activated receptor gamma induces cerebellar amyloid-beta levels and motor dysfunction in APP/PS1 transgenic mice. Biochem Biophys Res Commun 384(3):357-61. [PubMed: 19422805] [MGI Ref ID J:150592]
Du J; Sun B; Chen K; Zhang L; Liu S; Gu Q; Fan L; Zhao N; Wang Z. 2009. Metabolites of cerebellar neurons and hippocampal neurons play opposite roles in pathogenesis of Alzheimer's disease. PLoS ONE 4(5):e5530. [PubMed: 19436731] [MGI Ref ID J:148883]
Duffy AM; Holscher C. 2013. The incretin analogue D-Ala(2)GIP reduces plaque load, astrogliosis and oxidative stress in an APP/PS1 mouse model of Alzheimer's disease. Neuroscience 228:294-300. [PubMed: 23103794] [MGI Ref ID J:194003]
Fitz NF; Cronican AA; Saleem M; Fauq AH; Chapman R; Lefterov I; Koldamova R. 2012. Abca1 Deficiency Affects Alzheimer's Disease-Like Phenotype in Human ApoE4 But Not in ApoE3-Targeted Replacement Mice. J Neurosci 32(38):13125-36. [PubMed: 22993429] [MGI Ref ID J:188282]
Garcia-Alloza M; Borrelli LA; Hyman BT; Bacskai BJ. 2010. Antioxidants have a rapid and long-lasting effect on neuritic abnormalities in APP:PS1 mice. Neurobiol Aging 31(12):2058-68. [PubMed: 19124175] [MGI Ref ID J:168295]
Garcia-Alloza M; Borrelli LA; Rozkalne A; Hyman BT; Bacskai BJ. 2007. Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model J Neurochem 102(4):1095-104. [PubMed: 17472706] [MGI Ref ID J:120785]
Garcia-Alloza M; Robbins EM; Zhang-Nunes SX; Prucell SM; Betensky RA; Raju S; Prada C; Greenberg SM; Bacskai BJ; Frosch MP. 2006. Charaterization of amyloid deposition in the APPswe/PS2dE9 mouse model of Alzheimer disease Neurobiol Dis 24(3):516-524. [PubMed: 17029828] [MGI Ref ID J:113200]
Gimbel DA; Nygaard HB; Coffey EE; Gunther EC; Lauren J; Gimbel ZA; Strittmatter SM. 2010. Memory impairment in transgenic Alzheimer mice requires cellular prion protein. J Neurosci 30(18):6367-74. [PubMed: 20445063] [MGI Ref ID J:160557]
Goto Y; Niidome T; Hongo H; Akaike A; Kihara T; Sugimoto H. 2008. Impaired muscarinic regulation of excitatory synaptic transmission in the APPswe/PS1dE9 mouse model of Alzheimer's disease. Eur J Pharmacol 583(1):84-91. [PubMed: 18282567] [MGI Ref ID J:134791]
Halford RW; Russell DW. 2009. Reduction of cholesterol synthesis in the mouse brain does not affect amyloid formation in Alzheimer's disease, but does extend lifespan. Proc Natl Acad Sci U S A 106(9):3502-6. [PubMed: 19204288] [MGI Ref ID J:146447]
Hamilton A; Holscher C. 2012. The effect of ageing on neurogenesis and oxidative stress in the APP(swe)/PS1(deltaE9) mouse model of Alzheimer's disease. Brain Res 1449:83-93. [PubMed: 22418058] [MGI Ref ID J:183242]
He G; Luo W; Li P; Remmers C; Netzer WJ; Hendrick J; Bettayeb K; Flajolet M; Gorelick F; Wennogle LP; Greengard P. 2010. Gamma-secretase activating protein is a therapeutic target for Alzheimer's disease. Nature 467(7311):95-8. [PubMed: 20811458] [MGI Ref ID J:163997]
Heneka MT; Nadrigny F; Regen T; Martinez-Hernandez A; Dumitrescu-Ozimek L; Terwel D; Jardanhazi-Kurutz D; Walter J; Kirchhoff F; Hanisch UK; Kummer MP. 2010. Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine. Proc Natl Acad Sci U S A 107(13):6058-63. [PubMed: 20231476] [MGI Ref ID J:158919]
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Health & husbandry
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Colony Maintenance
Breeding & Husbandry When maintaining a live colony, hemizygotes may be bred with wildtype siblings. Coat color expected from breeding Black or Agouti. While the donating investigator warns that male aggression may require individual housing, there are no such reports of this problem to date in our colonies at The Jackson Laboratory (Jun 2006).
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