Strain Name:

C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax

Availability:

Repository- Live     Available at the JAX MMRRC

Use Restrictions Apply, see Terms of Use
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 C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/Mmjax MMRRC Stock Number 034843.
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. 007027) exhibit increasing expression of human amyloid beta precursor protein in the cortex, hippocampus, brain stem, and cerebellum with age. This mutant mouse strain may be useful in studies of Alzheimer's disease.

Description

Strain Information

Former Names C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/J    (Changed: 11-AUG-11 )
Type Coisogenic; Mutant Strain; Transgenic;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Mating SystemHomozygote x Homozygote         (Female x Male)   28-OCT-13
Specieslaboratory mouse
GenerationF?+1F13 (12-DEC-13)
Generation Definitions
 
Donating Investigator William Van Nostrand,   Stony Brook University

Description
These transgenic mice express neuronally derived human amyloid beta-precursor protein, APP gene, 770 isoform, containing the Swedish K670N/M671L, Dutch E693Q and Iowa D694N mutations, under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter. Mice hemizygous for the transgenic insert exhibit expression of human amyloid beta precursor protein in the cortex, hippocampus and brain stem with lower expression detected in the cerebellum. At age three months hemizygotes show a progressive accumulation of insoluble amyloid beta 40 and 42 peptides in brain tissue. The levels of accumulation of amyloid beta peptides is 12 to 14 fold higher in brain microvessels than in whole forebrain tissue homogenates. Fibrillar microvascular accumulations of amyloid beta peptides begin at approximately six months of age. Diffuse plaque-like deposits of amyloid beta that are similar to the plaques observed in human patients with the Dutch and Iowa familial disorders are initially detected at approximately 3 months of age in the subiculum, hippocampus and cortex. After six months of age the diffuse plaque-like deposits increase in number and spread to the olfactory bulb and thalamic region. Amyloid beta deposits are detected throughout the forebrain by 12 months of age. The donating investigator has made the strain homozygous and reports that mice homozygous for the transgenic insert are viable and fertile. This mutant mouse strain may be useful in studies of Alzheimer's disease and cerebral amyloid angiopathy.

Development
A transgenic construct containing 2.1kb of the human amyloid beta-precursor protein, APP gene, 770 isoform, with the Swedish K670N/M671L, Dutch E693Q and Iowa D694N mutations, under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter was injected into fertilized C57BL/6 mouse eggs. Founder line B was subsequently established and homozygotes generated.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at the MMRRC at The Jackson Laboratory. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 3 of 5 markers that determine C57BL/6J from C57BL/6N were found to be C57BL/6N. These data suggest the mice sent to the MMRRC at The Jackson Laboratory were on a mixed C57BL/6J ; C57BL/6N genetic background.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

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006006   B6.Cg-Tg(Prnp-APP)A-2Dbo/J
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006005   B6.Cg-Tg(Prnp-App/APPswe)E1-2Dbo/Mmjax
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008333   B6;129P2-Dldtm1Ptl/J
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005086   C57BL/6-Tg(Camk2a-MME)3Selk/J
008833   C57BL/6-Tg(Camk2a-UBB)3413-1Fwvl/J
010800   C57BL/6-Tg(Thy1-PTGS2)300Kand/J
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View Alzheimer's Disease Models     (109 strains)

Strains carrying   Tg(Thy1-APPSwDutIowa)BWevn allele
009126   B6.Cg-Nos2tm1Lau Tg(Thy1-APPSwDutIowa)BWevn/Mmjax
View Strains carrying   Tg(Thy1-APPSwDutIowa)BWevn     (1 strain)

View Strains carrying other alleles of APP     (15 strains)

Strains carrying other alleles of Thy1
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001317   B6.Cg-Gpi1a Thy1a Igha/J
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022073   B6.Cg-Rag1tm1Mom Thy1a Tg(Tcra2C,Tcrb2C)1Dlo/J
014550   B6.Cg-Thy1a Tg(TcraCWM5,TcrbCWM5)1807Wuth/J
005023   B6.Cg-Thy1a/Cy Tg(TcraTcrb)8Rest/J
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007901   B6.Cg-Tg(Thy1-Brainbow1.0)HLich/J
007911   B6.Cg-Tg(Thy1-Brainbow1.1)MLich/J
007921   B6.Cg-Tg(Thy1-Brainbow2.1)RLich/J
003710   B6.Cg-Tg(Thy1-CFP)23Jrs/J
014131   B6.Cg-Tg(Thy1-CFP)IJrs/GfngJ
007940   B6.Cg-Tg(Thy1-CFP/COX8A)C1Lich/J
007967   B6.Cg-Tg(Thy1-CFP/COX8A)S2Lich/J
012597   B6.Cg-Tg(Thy1-COL25A1)861Yfu/J
007612   B6.Cg-Tg(Thy1-COP4/EYFP)18Gfng/J
007615   B6.Cg-Tg(Thy1-COP4/EYFP)9Gfng/J
013161   B6.Cg-Tg(Thy1-Clomeleon)1Gjau/J
007919   B6.Cg-Tg(Thy1-EGFP)OJrs/GfngJ
005630   B6.Cg-Tg(Thy1-EYFP)15Jrs/J
009611   B6.Cg-Tg(Thy1-Nlgn1)6Hnes/J
009612   B6.Cg-Tg(Thy1-Nlgn2)6Hnes/J
021069   B6.Cg-Tg(Thy1-PA-GFP)5Rmpl/J
021070   B6.Cg-Tg(Thy1-PA-GFP)6Rmpl/J
003709   B6.Cg-Tg(Thy1-YFP)16Jrs/J
003782   B6.Cg-Tg(Thy1-YFP)HJrs/J
005627   B6.Cg-Tg(Thy1-YFP/Syp)10Jrs/J
007606   B6.Cg-Tg(Thy1-cre/ERT2,-EYFP)AGfng/J
025854   B6.FVB-Ptprca Tg(CAG-luc,-GFP)L2G85Chco Thy1a/J
000406   B6.PL-Thy1a/CyJ
000983   B6.PL/(84NS)CyJ
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007910   B6;CBA-Tg(Thy1-Brainbow1.0)LLich/J
011070   B6;CBA-Tg(Thy1-EGFP)SJrs/NdivJ
017892   B6;CBA-Tg(Thy1-GCaMP2.2c)8Gfng/J
017893   B6;CBA-Tg(Thy1-GCaMP3)6Gfng/J
014130   B6;CBA-Tg(Thy1-YFP)GJrs/GfngJ
014651   B6;CBA-Tg(Thy1-spH)21Vnmu/J
015814   B6;CBA-Tg(Thy1-spH)64Vnmu/FrkJ
012341   B6;SJL-Tg(Thy1-COP3/EYFP)1Gfng/J
012344   B6;SJL-Tg(Thy1-COP3/EYFP)4Gfng/J
012348   B6;SJL-Tg(Thy1-COP3/EYFP)8Gfng/J
012350   B6;SJL-Tg(Thy1-COP4*H134R/EYFP)20Gfng/J
008004   B6;SJL-Tg(Thy1-ECFP/VAMP2)1Sud/J
012836   B6;SJL-Tg(Thy1-TARDBP)4Singh/J
007610   B6;SJL-Tg(Thy1-cre/ERT2,-EYFP)VGfng/J
012332   B6;SJL-Tg(Thy1-hop/EYFP)2Gfng/J
012334   B6;SJL-Tg(Thy1-hop/EYFP)4Gfng/J
006554   B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
025401   B6SJL-Tg(Thy1-COX8A/Dendra)57Gmnf/J
017590   B6SJL-Tg(Thy1-DCTN1*G59S)M2Pcw/J
007880   B6SJL-Tg(Thy1-Stx1a/EYFP)1Sud/J
007856   B6SJL-Tg(Thy1-Syt1/ECFP)1Sud/J
017589   B6SJL-Tg(Thy1-TARDBP*G298S)S97Pcw/J
017351   BKa.Cg-Ptprcb Bmi1tm1Ilw Thy1a/J
007687   BKa.Cg-Sox17tm1Sjm Ptprcb Thy1a/J
007686   BKa.Cg-Sox17tm2Sjm Ptprcb Thy1a/J
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010703   C57BL/6-Tg(Thy1-PTGS2)303Kand/J
012769   C57BL/6-Tg(Thy1-Sncg)HvP36Putt/J
024339   C57BL/6J-Tg(Thy1-GCaMP6f)GP5.11Dkim/J
025393   C57BL/6J-Tg(Thy1-GCaMP6f)GP5.17Dkim/J
024276   C57BL/6J-Tg(Thy1-GCaMP6f)GP5.5Dkim/J
025776   C57BL/6J-Tg(Thy1-GCaMP6s)GP4.12Dkim/J
024275   C57BL/6J-Tg(Thy1-GCaMP6s)GP4.3Dkim/J
025533   C57BL/6N-Sncatm1Mjff Tg(Thy1-SNCA)15Mjff/J
016936   C57BL/6N-Tg(Thy1-SNCA)12Mjff/J
017682   C57BL/6N-Tg(Thy1-SNCA)15Mjff/J
005307   CBy.Cg-Thy1a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ
005922   CBy.Cg-Thy1a Tg(TcraCl1,TcrbCl1)1Shrm/J
005443   CBy.PL(B6)-Thy1a/ScrJ
024704   D2.Cg-Gpnmb+Tg(Thy1-CFP)23Jrs/SjJ
025018   D2.Cg-Gpnmb+Tg(Thy1-YFP)HJrs/SjJ
018671   D2.Cg-Tg(Thy1-CFP)23Jrs/SjJ
024705   D2.Cg-Tg(Thy1-YFP)HJrs/SjJ
025019   D2.Cg-Tg(Thy1-YFP/Syp)10Jrs/SjJ
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006143   FVB/N-Tg(Thy1-cre)1Vln/J
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005686   NOD.Cg-Thy1a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ
004483   NOD.NON-Thy1a/1LtJ
002721   NOD.NON-Thy1a/J
005651   SJL.AK-Thy1a/TseJ
003961   SJL.Cg Thy1a-Noxo1hslt/J
021226   STOCK Tg(Thy1-Brainbow3.1)18Jrs/J
021225   STOCK Tg(Thy1-Brainbow3.1)3Jrs/J
021227   STOCK Tg(Thy1-Brainbow3.2)7Jrs/J
013162   STOCK Tg(Thy1-Clomeleon)12Gjau/J
013163   STOCK Tg(Thy1-Clomeleon)13Gjau/J
007788   STOCK Tg(Thy1-EGFP)MJrs/J
012708   STOCK Tg(Thy1-cre/ERT2,-EYFP)HGfng/PyngJ
View Strains carrying other alleles of Thy1     (92 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
Cerebral Amyloid Angiopathy, App-Related
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Tg(Thy1-APPSwDutIowa)BWevn/0

        involves: C57BL/6
  • nervous system phenotype
  • abnormal astrocyte morphology
    • astrocyte numbers and density are enhanced in thalamic and cortical regions where fibrillar amyloid beta deposits are prominent   (MGI Ref ID J:124911)
  • abnormal microglial cell physiology
    • activation of microglial and astrocytes is elevated in cortex   (MGI Ref ID J:124911)
    • microglial cells show significantly increased levels of complement proteins C1q, C3 and C4   (MGI Ref ID J:124911)
  • amyloid beta deposits
    • over the course of 1 year, progressive and robust accumulation of insoluble amyloid beta-40 and -42 peptides is observed in mouse brains; increase in peptides is first observed at 3 months and increases markedly by 12 months   (MGI Ref ID J:89848)
    • soluble and insoluble amyloid beta-40 peptide levels are 10-fold higher than amyloid beta-42 peptide levels   (MGI Ref ID J:89848)
    • amyloid beta deposits are observed in the regions of the subiculum, hippocampus, and cortex at ~3 months; by ~6 months deposits become more numerous and appear in the olfactory bulb and thalamic region as well, with deposits throughout most of the forebrain by 12 months   (MGI Ref ID J:89848)
    • parenchymal amyloid deposits mainly present as diffuse, plaque-like deposits, with occasional deposits having a more compact structure suggesting a fibrillar nature   (MGI Ref ID J:89848)
    • deposits are largely in parenchyma and in diffuse form in cortex   (MGI Ref ID J:124911)
  • cerebral amyloid angiopathy
    • levels of amyloid beta-40 and -42 peptides are 12- and 14-fold higher in forebrain microvessels than in whole forebrain homogenates at 12 months of age; at ~3 months, levels in vasculature of forebrains is higher than whole forebrain tissue   (MGI Ref ID J:89848)
    • vascular amyloid beta accumulation is prominent in the thalamus and subiculum, and increases with age such that 45-55% of vessels are affected at 12 months of age; at ~6 months of age, amyloid beta deposits in and around microvessels in the thalamus and subiculum are observed   (MGI Ref ID J:89848)
    • microvascular amyloid beta accumulations are mainly fibrillar   (MGI Ref ID J:89848)
    • some arterioles in these brain regions show strong vascular and perivascular amyloid beta depostion, while blood vessel-rich regions like the hippocampal fissure show large accumulations of perivascular amyloid beta   (MGI Ref ID J:89848)
    • evidence of microhemorrhage is observed in microvessels with amyloid beta deposits   (MGI Ref ID J:89848)
    • microvascular fibrillar amyloid beta accumulation is observed in thalamic and hippocampal regions   (MGI Ref ID J:124911)
  • immune system phenotype
  • abnormal microglial cell physiology
    • activation of microglial and astrocytes is elevated in cortex   (MGI Ref ID J:124911)
    • microglial cells show significantly increased levels of complement proteins C1q, C3 and C4   (MGI Ref ID J:124911)
  • cardiovascular system phenotype
  • abnormal blood circulation
    • reduced cerebral blood flow, CBF, response (21% increase) to whisker stimulation is observed relative to controls (38% increase) at 9 months   (MGI Ref ID J:119251)
    • with myocardin gene transfer, CBF response drops to 10% in transgenic mice, a decrease of 50%, while it increased to 27% with shSRF gene transfer compared to 19% in shGFP controls   (MGI Ref ID J:119251)
  • hematopoietic system phenotype
  • abnormal microglial cell physiology
    • activation of microglial and astrocytes is elevated in cortex   (MGI Ref ID J:124911)
    • microglial cells show significantly increased levels of complement proteins C1q, C3 and C4   (MGI Ref ID J:124911)
  • homeostasis/metabolism phenotype
  • amyloidosis
    • mutants show decreased clearance of the mutant form of amyloid beta peptides compared to wild-type amyloid beta   (MGI Ref ID J:89848)
    • amyloid beta deposits
      • over the course of 1 year, progressive and robust accumulation of insoluble amyloid beta-40 and -42 peptides is observed in mouse brains; increase in peptides is first observed at 3 months and increases markedly by 12 months   (MGI Ref ID J:89848)
      • soluble and insoluble amyloid beta-40 peptide levels are 10-fold higher than amyloid beta-42 peptide levels   (MGI Ref ID J:89848)
      • amyloid beta deposits are observed in the regions of the subiculum, hippocampus, and cortex at ~3 months; by ~6 months deposits become more numerous and appear in the olfactory bulb and thalamic region as well, with deposits throughout most of the forebrain by 12 months   (MGI Ref ID J:89848)
      • parenchymal amyloid deposits mainly present as diffuse, plaque-like deposits, with occasional deposits having a more compact structure suggesting a fibrillar nature   (MGI Ref ID J:89848)
      • deposits are largely in parenchyma and in diffuse form in cortex   (MGI Ref ID J:124911)
    • cerebral amyloid angiopathy
      • levels of amyloid beta-40 and -42 peptides are 12- and 14-fold higher in forebrain microvessels than in whole forebrain homogenates at 12 months of age; at ~3 months, levels in vasculature of forebrains is higher than whole forebrain tissue   (MGI Ref ID J:89848)
      • vascular amyloid beta accumulation is prominent in the thalamus and subiculum, and increases with age such that 45-55% of vessels are affected at 12 months of age; at ~6 months of age, amyloid beta deposits in and around microvessels in the thalamus and subiculum are observed   (MGI Ref ID J:89848)
      • microvascular amyloid beta accumulations are mainly fibrillar   (MGI Ref ID J:89848)
      • some arterioles in these brain regions show strong vascular and perivascular amyloid beta depostion, while blood vessel-rich regions like the hippocampal fissure show large accumulations of perivascular amyloid beta   (MGI Ref ID J:89848)
      • evidence of microhemorrhage is observed in microvessels with amyloid beta deposits   (MGI Ref ID J:89848)
      • microvascular fibrillar amyloid beta accumulation is observed in thalamic and hippocampal regions   (MGI Ref ID J:124911)
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

APP related

Neurobiology Research
Alzheimer's Disease
Neurodegeneration

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Tg(Thy1-APPSwDutIowa)BWevn
Allele Name transgene insertion B, William E Van Nostrand
Allele Type Transgenic (Inserted expressed sequence)
Common Name(s) APPSwDI; Tg-SwDI; Tg-SwDI/B;
Mutation Made By William Van Nostrand,   Stony Brook University
Strain of OriginC57BL/6
Expressed Gene APP, amyloid beta (A4) precursor protein, human
Promoter Thy1, thymus cell antigen 1, theta, mouse, laboratory
Molecular Note A transgenic construct containing 2.1kb of the human amyloid beta-precursor protein, APP gene, 770 isoform, with the Swedish K670N/M671L, Dutch E693Q and Iowa D694N mutations, under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter was injected into fertilized C57BL/6 mouse eggs. Founder line B was subsequently established and homozygotes generated. Human amyloid beta precursor protein expression is detected in the brains of transgenic mice. Two other lines, A anc C were also generated, with line A having similar levels of transgene expression and amyloid beta accumulation to line B while line C has 2-fold higher expression of human Amyloid beta-precursor protein and shows 4-fold higher accumulations of soluble and insoluble AB peptides in the brain. [MGI Ref ID J:89848]
 
 

Genotyping

Genotyping Information

Genotyping Protocols

Generic Tg(APP), Standard PCR
Tg(APP), Separated QPCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Davis J; Xu F; Deane R; Romanov G; Previti ML; Zeigler K; Zlokovic BV; Van Nostrand WE. 2004. Early-onset and robust cerebral microvascular accumulation of amyloid beta-protein in transgenic mice expressing low levels of a vasculotropic Dutch/Iowa mutant form of amyloid beta-protein precursor. J Biol Chem 279(19):20296-306. [PubMed: 14985348]  [MGI Ref ID J:89848]

Additional References

Tg(Thy1-APPSwDutIowa)BWevn related

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]

Carrasco J; Adlard P; Cotman C; Quintana A; Penkowa M; Xu F; Van Nostrand WE; Hidalgo J. 2006. Metallothionein-I and -III expression in animal models of Alzheimer disease. Neuroscience 143(4):911-22. [PubMed: 17027170]  [MGI Ref ID J:117948]

Chow N; Bell RD; Deane R; Streb JW; Chen J; Brooks A; Van Nostrand W; Miano JM; Zlokovic BV. 2007. Serum response factor and myocardin mediate arterial hypercontractility and cerebral blood flow dysregulation in Alzheimer's phenotype. Proc Natl Acad Sci U S A 104(3):823-8. [PubMed: 17215356]  [MGI Ref ID J:119251]

Colton CA; Wilcock DM; Wink DA; Davis J; Van Nostrand WE; Vitek MP. 2008. The effects of NOS2 gene deletion on mice expressing mutated human AbetaPP. J Alzheimers Dis 15(4):571-87. [PubMed: 19096157]  [MGI Ref ID J:143551]

Davis J; Xu F; Miao J; Previti ML; Romanov G; Ziegler K; Van Nostrand WE. 2006. Deficient cerebral clearance of vasculotropic mutant Dutch/Iowa Double Ass in human AssPP transgenic mice. Neurobiol Aging 27(7):946-54. [PubMed: 16105708]  [MGI Ref ID J:108851]

Dhurandhar EJ; Allison DB; van Groen T; Kadish I. 2013. Hunger in the absence of caloric restriction improves cognition and attenuates Alzheimer's disease pathology in a mouse model. PLoS One 8(4):e60437. [PubMed: 23565247]  [MGI Ref ID J:200150]

Fan R; Defilippis K; Van Nostrand WE. 2007. Induction of complement proteins in a mouse model of cerebral microvascular Abeta deposition. J Neuroinflammation 4(1):22. [PubMed: 17877807]  [MGI Ref ID J:124911]

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]

Hirsch-Reinshagen V; Maia LF; Burgess BL; Blain JF; Naus KE; McIsaac SA; Parkinson PF; Chan JY; Tansley GH; Hayden MR; Poirier J; Van Nostrand W; Wellington CL. 2005. The absence of ABCA1 decreases soluble ApoE levels but does not diminish amyloid deposition in two murine models of Alzheimer disease. J Biol Chem 280(52):43243-56. [PubMed: 16207707]  [MGI Ref ID J:105900]

Hutchinson D; Ho V; Dodd M; Dawson HN; Zumwalt AC; Schmitt D; Colton CA. 2007. Quantitative measurement of postural sway in mouse models of human neurodegenerative disease. Neuroscience 148(4):825-32. [PubMed: 17764851]  [MGI Ref ID J:128390]

Liao MC; Van Nostrand WE. 2010. Degradation of soluble and fibrillar amyloid beta-protein by matrix metalloproteinase (MT1-MMP) in vitro. Biochemistry 49(6):1127-36. [PubMed: 20050683]  [MGI Ref ID J:159886]

Medeiros R; Kitazawa M; Caccamo A; Baglietto-Vargas D; Estrada-Hernandez T; Cribbs DH; Fisher A; Laferla FM. 2011. Loss of muscarinic m(1) receptor exacerbates Alzheimer's disease-like pathology and cognitive decline. Am J Pathol 179(2):980-91. [PubMed: 21704011]  [MGI Ref ID J:174403]

Miao J; Vitek MP; Xu F; Previti ML; Davis J; Van Nostrand WE. 2005. Reducing cerebral microvascular amyloid-beta protein deposition diminishes regional neuroinflammation in vasculotropic mutant amyloid precursor protein transgenic mice. J Neurosci 25(27):6271-7. [PubMed: 16000616]  [MGI Ref ID J:99430]

Miao J; Xu F; Davis J; Otte-Holler I; Verbeek MM; Van Nostrand WE. 2005. Cerebral Microvascular Amyloid {beta} Protein Deposition Induces Vascular Degeneration and Neuroinflammation in Transgenic Mice Expressing Human Vasculotropic Mutant Amyloid {beta} Precursor Protein. Am J Pathol 167(2):505-15. [PubMed: 16049335]  [MGI Ref ID J:99946]

Passos GF; Medeiros R; Cheng D; Vasilevko V; Laferla FM; Cribbs DH. 2013. The Bradykinin B1 Receptor Regulates Abeta Deposition and Neuroinflammation in Tg-SwDI Mice. Am J Pathol 182(5):1740-9. [PubMed: 23470163]  [MGI Ref ID J:195541]

Ridnour LA; Dhanapal S; Hoos M; Wilson J; Lee J; Cheng RY; Brueggemann EE; Hines HB; Wilcock DM; Vitek MP; Wink DA; Colton CA. 2012. Nitric oxide-mediated regulation of beta-amyloid clearance via alterations of MMP-9/TIMP-1. J Neurochem 123(5):736-49. [PubMed: 23016931]  [MGI Ref ID J:190735]

Van Vickle GD; Esh CL; Daugs ID; Kokjohn TA; Kalback WM; Patton RL; Luehrs DC; Walker DG; Lue LF; Beach TG; Davis J; Van Nostrand WE; Castano EM; Roher AE. 2008. Tg-SwDI transgenic mice exhibit novel alterations in AbetaPP processing, Abeta degradation, and resilient amyloid angiopathy. Am J Pathol 173(2):483-93. [PubMed: 18599612]  [MGI Ref ID J:137886]

Wilcock DM; Gharkholonarehe N; Van Nostrand WE; Davis J; Vitek MP; Colton CA. 2009. Amyloid reduction by amyloid-beta vaccination also reduces mouse tau pathology and protects from neuron loss in two mouse models of Alzheimer's disease. J Neurosci 29(25):7957-65. [PubMed: 19553436]  [MGI Ref ID J:150418]

Wilcock DM; Lewis MR; Van Nostrand WE; Davis J; Previti ML; Gharkholonarehe N; Vitek MP; Colton CA. 2008. Progression of amyloid pathology to Alzheimer's disease pathology in an amyloid precursor protein transgenic mouse model by removal of nitric oxide synthase 2. J Neurosci 28(7):1537-45. [PubMed: 18272675]  [MGI Ref ID J:132221]

Wilcock DM; Vitek MP; Colton CA. 2009. Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer's disease. Neuroscience 159(3):1055-69. [PubMed: 19356689]  [MGI Ref ID J:148938]

Xu F; Grande AM; Robinson JK; Previti ML; Vasek M; Davis J; Van Nostrand WE. 2007. Early-onset subicular microvascular amyloid and neuroinflammation correlate with behavioral deficits in vasculotropic mutant amyloid beta-protein precursor transgenic mice. Neuroscience 146(1):98-107. [PubMed: 17331655]  [MGI Ref ID J:122063]

Xu F; Vitek MP; Colton CA; Previti ML; Gharkholonarehe N; Davis J; Van Nostrand WE. 2008. Human apolipoprotein E redistributes fibrillar amyloid deposition in Tg-SwDI mice. J Neurosci 28(20):5312-20. [PubMed: 18480287]  [MGI Ref ID J:136318]

Zeng Y; Callaghan D; Xiong H; Yang Z; Huang P; Zhang W. 2012. Abcg2 deficiency augments oxidative stress and cognitive deficits in Tg-SwDI transgenic mice. J Neurochem :. [PubMed: 22578166]  [MGI Ref ID J:186567]

Zhang L; Dasuri K; Fernandez-Kim SO; Bruce-Keller AJ; Freeman LR; Pepping JK; Beckett TL; Murphy MP; Keller JN. 2013. Prolonged diet induced obesity has minimal effects towards brain pathology in mouse model of cerebral amyloid angiopathy: implications for studying obesity-brain interactions in mice. Biochim Biophys Acta 1832(9):1456-62. [PubMed: 23313575]  [MGI Ref ID J:202444]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice may be bred as homozygotes.
Mating SystemHomozygote x Homozygote         (Female x Male)   28-OCT-13

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