Search Criteria: Research Area is "Neurobiology Research: Alzheimer's Disease (strains expressing mutant APP)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 004462 | B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J | Level 4 |
| 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 develo
..... For more information please see the full descriiption on the strain data sheet | ||
| 006409 | 129S1.129(Cg)-Tg(APPSw)40Btla/J | Repository- Live |
| These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the wild-type mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics wild-type mouse gene expression patterns. These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.
Of note, this is one of two 129S1/SvImJ congenic R1.40 transgenic strains (129S1-R1.40) segregating for transgene copy number; one with lower trangene copy number (Stock No. 006409) and one with higher transgene copy number (Stock No. 008609). At the
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| 006555 | A.129(B6)-Tg(APPSw)40Btla/J | Repository- Live |
| These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. The donating investigator reports increased mortality in young homozygous animals (higher incidence in females). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could va
..... | ||
| 005300 | B6.129-Tg(APPSw)40Btla/J | Repository- Live |
| These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is two to three fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. Levels of the beta- secretase generated human APP derivative, C-terminal 13.5kDA fragment, are elevated in brain tissue. ELISA enzyme-linked immunosorbent assay (ELISA) analysis of brain homogenates show a significant increase in total amyloid-beta peptides and 42 amino acid length amyloid beta peptides. By 14 months of age, homozygous mice develop both parenchymal and vascular amyloid beta deposits, which first appear in the frontal cortex and then spread into the hippocampus. The donating investigat
..... For more information please see the full descriiption on the strain data sheet | ||
| 006406 | B6.129S4-Tg(APPSwLon)96Btla/J | Repository- Live |
| Mice hemizygous for this "K670N/M671L + V717I" mutant APP YAC transgene are viable and fertile. RT-PCR analysis shows hemizygous mice express the mutant human APP mRNA at levels similar to endogenous mouse in brain and peripheral tissues. Further, transcript levels of the most common alternative splice variants (encoding human APP-695, -751 and -770) parallel the endogenous mouse gene expression. The levels of total amyloid-beta and longer amyloid-beta peptides (species terminating at amino acids 42/43) are elevated compared to wildtype mice, but not to the extent as observed in a similar strain carrying only the APP (K670N/M671L) mutant transgene (see Stock No. 005300). These mice may be useful in studies of the pathogenesis of Familial Alzheimer’s Disease, specifically focusing on the importance of processing at the gamma-secretase site to elevate levels of amyloid-beta 1-42(43). | ||
| 005866 | B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/J | Repository- Live |
| Double transgenic mice are viable and fertile. At 6 months of age, double-transgenic mice show visible amyloid plaque deposition but are indistinguishable from nontransgenic animals in all cognitive measures. By 18 months, amyloid deposits were much higher in APPswe/PS1dE9 mice with statistically significant but mild decreases in cholinergic markers (cortex and hippocampus) and somatostatin levels (cortex). Performance of older double-transgenic mice is impaired in all cognitive tasks, and deficits in episodic-like memory tasks correlate with total amyloid-beta peptide loads in the brain. | ||
| 005864 | B6.Cg-Tg(APPswe,PSEN1dE9)85Dbo/J | Repository- Live |
| 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 tra
..... For more information please see the full descriiption on the strain data sheet | ||
| 006293 | B6.Cg-Tg(PDGFB-APPSwInd)20Lms/2J | Repository- Live |
| 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. This mutant mouse strain represents a model that may be useful in studies of the pathogenesis of Familial Alzheim
..... For more information please see the full descriiption on the strain data sheet | ||
| 006005 | B6.Cg-Tg(Prnp-App/APPswe)E1-2Dbo/J | Repository- Live |
| These transgenic mice express a chimeric mouse/human amyloid precursor protein (APPswe) under the control of the mouse prion protein promoter. Mice that are hemizygous for the transgene are viable and fertile. More than half of the female hemizygous mice do not survive past 15 months of age. This mutant mouse strain may be useful in studies of Alzheimer's Disease. | ||
| 007051 | B6.Cg-Tg(tetO-APPSwInd)102Dbo/J | Repository- Live |
| Hemizygotes for this tetO-APPswe/ind transgene are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP695) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APP695swe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the control of a tissue-specific promoter, APP695swe/ind expression in the appropriate tissues of the bitransgenic offspring can be regulated with the tetracycline analog doxycycline (dox). These tetO-APPswe/ind transgenic mice may be useful in studies of Alzheimer's disease and other neurodegenerative tauopathies. For example, when bred to a strain expressing tTA in brain tissues (see Stock No. For more information please see the full descriiption on the strain data sheet | ||
| 007052 | B6.Cg-Tg(tetO-APPSwInd)107Dbo/J | Repository- Live |
| Hemizygotes for this tetO-APPswe/ind transgene are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP695) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APP695swe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, APP695swe/ind expression in the target tissue of the bitransgenic offspring can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring.
These tetO-APPswe/ind transgenic mice may be useful in studies of Alzheimer's disease and other neurodegenerative tauopathies. For example, when bred to a strain expressing tTA in brain tissues (see Stock No.
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| 007049 | B6.Cg-Tg(tetO-APPSwInd)885Dbo/J | Repository- Live |
| Hemizygotes for this tetO-APPswe/ind transgene are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP695) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APP695swe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, APP695swe/ind expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog doxycycline (dox). These tetO-APPswe/ind transgenic mice may be useful in studies of Alzheimer's disease and other neurodegenerative tauopathies. For example, when bred to a strain expressing tTA in brain tissues (see Stock No. For more information please see the full descriiption on the strain data sheet | ||
| 006880 | B6;C3-Tg(Prnp-ITM2B/APP695*40)1Emcg/J | Repository- Live |
| Mice hemizygous for this BRI-Abeta40 transgene are viable and fertile with a normal life span and no obvious behavioral abnormalities. Transgenic BRI-Abeta mRNA is expressed in a pattern characteristic of the mouse prion protein promoter; highest expression levels are detected in the cerebellar granule cells and hippocampus, followed by the cortex, pons, thalamus, and midbrain. Wildtype BRI protein is cleaved by furin or a furin-like protease near the COOH-terminus which releases a soluble 23 amino acid peptide. In the transgenic fusion protein, Abeta1-40 is fused to the C terminus of the BRI protein at the furin-like cleavage site such that cleavage results in efficient Abeta1-40 secretion into the lumen or extracellular space. Therefore, these mice specifically express the Abeta1-40 isoform in the absence of human amyloid beta protein precursor (APP) overexpression. In contrast to BRI-Abeta42 transgenic mice (Stock No. 007002),
..... For more information please see the full descriiption on the strain data sheet | ||
| 007002 | B6;C3-Tg(Prnp-ITM2B/APP695*42)A12Emcg/J | Repository- Live |
| Mice hemizygous for this BRI-Abeta42 transgene are viable and fertile with a normal lifespan and no obvious behavioral abnormalities. Transgenic BRI-Abeta42 mRNA is expressed in a pattern characteristic of the mouse prion protein promoter; highest transgene expression levels are detected in the cerebellar granule cells and hippocampus, followed by the cortex, pons, thalamus, and midbrain. Wildtype BRI protein is cleaved by furin or a furin-like protease near the COOH-terminus which releases a soluble 23 amino acid peptide. In the transgenic fusion protein, Abeta1-42 is fused to the C terminus of the BRI protein at the furin-like cleavage site such that cleavage results in efficient Abeta1-42 secretion into the lumen or extracellular space. Therefore, these mice specifically express the Abeta1-42 isoform in the absence of human amyloid beta protein precursor (APP) overexpression. In contrast to BRI-Abeta40 transgenic mice (Stock No. 00
..... For more information please see the full descriiption on the strain data sheet | ||
| 006004 | B6C3-Tg(tetO-APPSwInd)885Dbo/J | Repository- Live |
| Hemizygous mice are viable and fertile. These transgenic mice express a chimeric mouse/human amyloid precursor protein (APP) bearing the Swedish (KM570/571NL) and Indiana (V617F) mutations associated with Alzheimer's disease (APPswe/ind) under the control of a tetracycline-responsive promoter element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters , APPswe/ind transgene expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. When bred to a strain expressing rtTA or tTA in brain tissues (see Stock No. 003010, for example), this mutant mouse strain may be useful in studies of Alzheimer's Disease. | ||
| 006554 | B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/J | Repository- Live |
| 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. 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. In addition, these mice have reduced synaptic marker protein levels, increased p25 levels, neuron loss, and memory impairment in the Y-maze test. 5XFA
..... For more information please see the full descriiption on the strain data sheet | ||
| 007027 | C57BL/6-Tg(Thy1-APPSwDutIowa)BWevn/J | Repository- Live |
| 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 initiall
..... For more information please see the full descriiption on the strain data sheet | ||
| 006472 | D2.129(B6)-Tg(APPSw)40Btla/J | Repository- Live |
| These R1.40 transgenic mice express all mRNA and protein isoforms of the human amyloid beta (A4) precursor protein APP containing the Familial Alzheimer's Disease (FAD) Swedish mutation K670N/M671L. Transgene expression (mRNA and full-length protein) is 2 to 3 fold the endogenous mouse App expression level in the hemizygous state in brain tissue as revealed by RT-PCR and Western Blot analysis. Transgene expression pattern mimics endogenous mouse gene expression patterns. The donating investigator reports increased mortality in young homozygous animals (higher incidence in females). These R1.40 transgenic mice may be useful in studying the pathogenesis of Familial Alzheimer's Disease and possible therapeutic treatments.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could va
..... | ||
| 003378 | B6C3-Tg(APP695)3Dbo Tg(PSEN1)5Dbo/J | Repository-Cryopreserved |
| These transgenic mice express human presenilin 1 (A246E variant) and a chimeric amyloid precursor protein (APPSwe). The mouse prion protein promoter directs expression of both transgenes. Elevated levels of the AB1-42(43) peptide is detected in brain homogenates. By nine months of age, histological examination of brain tissue reveals numerous amyloid deposits resembling those observed in the brains of patients with Alzheimer's disease (AD). The number of amyloid deposits increases dramatically between the ages of 10 and 12 months. These mice provide a useful model for studying the underlying mechanism of amyloid deposition, a process implicated in AD. | ||
| 003375 | C3B6-Tg(APP695)3Dbo/J | Repository-Cryopreserved |
| These transgenic mice express the human amyloid precursor protein bearing the Swedish (K670N/M671L) mutation and develop amyloid deposits in brain tissue by 18-20 months of age. These mice provide a useful model for studying the underlying mechanism of amyloid deposition, a process implicated in Alzheimer's disease (AD). | ||
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