JAX
Mouse Strain Datasheet
B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/Mmjax
Also Known As: APPswe/PS1dE9, APPswe line C3-3 x PS1dE9 line S-9
These double-transgenic mice show increased amyloid plaque deposition with age along with deficits in cognitive tasks and episodic-like memory tasks.
Donating Investigator
Dr. David R Borchelt, University of Florida
Genetic overview
| Genetic Background | Generation |
|---|---|
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Tg(APP695)3Dbo
| Allele Type |
|---|
| Transgenic (Humanized sequence, Inserted expressed sequence) |
Tg(PSEN1dE9)S9Dbo
| Allele Type |
|---|
| Transgenic (Humanized sequence, Inserted expressed sequence) |
Detailed Description
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. Mutant mice, hemizygous for each transgene, and on the C57BL/6J background (N6), have altered EEG (decreased cortical theta activity and increased beta and gamma activity). EEG differences are detected as early as 7 month of age (Wang et al. Brain Res 2002).
Development
Mutant amyloid precursor protein (APPswe) transgenic mice (line C3-3) express a chimeric mouse/human APP-695 with mutations linked to familial Alzheimers disease (KM 593/594 NL; also called K670N/M671L). The C3-3 line was backcrossed to C57BL/6J mice for 10 generations. Presenilin 1 (PSEN1) transgenic mice (line S-9) express human PSEN1 carrying the exon-9-deleted variant (PSEN1dE9) associated with familial Alzheimer's disease. Originally created on a hybrid strain background (C3H/HeJ;C57BL/6J), the S-9 line was backcrossed to C57BL/6J for six generations. Both are under the control of the mouse prion protein (PrP) promoter, directing transgene expression predominantly to CNS neurons. APPswe/PS1dE9 double transgenic mice were produced by mating APP-695 line C3-3 males to PS1dE9 line S-9 females, and then backcrossing double transgenic males to C57BL/6J mice for 10 generations before arriving at the MMRRC at The Jackson Laboratory.
Expression Data
| Expressed Gene | APP695, amyloid beta (A4) precursor protein (chimeric), mouse/human chimera |
|---|---|
| Site of Expression | |
| Expressed Gene | PSEN1, presenilin 1, human |
| Site of Expression |
Control Suggestions
Selected References
- Savonenko A; Xu GM; Melnikova T; Morton JL; Gonzales V; Wong MP; Price DL; Tang F; Markowska AL; Borchelt DR. 2005. Episodic-like memory deficits in the APPswe/PS1dE9 mouse model of Alzheimer's disease: relationships to beta-amyloid deposition and neurotransmitter abnormalities. Neurobiol Dis 18(3):602-17. PubMed: 15755686MGI: J:104236
Tg(APP695)3Dbo
Allele Symbol: Tg(APP695)3Dbo
| Allele Name | transgene insertion 3, David R Borchelt |
|---|---|
| Allele Type | Transgenic (Humanized sequence, Inserted expressed sequence) |
| Allele Synonym(s) | APP695; APP695swe; APPswe; Mo/HuAPPswe; line C3-3 |
| Gene Symbol and Name | Tg(APP695)3Dbo, transgene insertion 3, David R Borchelt |
| Gene Synonym(s) | APP695; APP695swe; APPswe; Mo/HuAPPswe; line C3-3 |
| Promoter | Prn, prion protein readthrough transcript, mouse, laboratory |
| Expressed Gene | APP695, amyloid beta (A4) precursor protein (chimeric), mouse/human chimera |
| Strain of Origin | (C57BL/6J x C3H/HeJ)F2 |
| Chromosome | UN |
| General Note | Three transgenic lines were generated and designated by the authors lines Q2-2, E1-2 (Tg(Prnp-App/APPswe)E1-2Dbo) and C3-3. This line was generated from founder number C3-3. Transgenic mice develop amyloid deposits in brain tissue by 18-20 months of age. Transgenic mice that are also transgenic for Tg(PSEN1)5Dboexpress both human presenilin 1 (A246E variant) and a chimeric amyloid precursor protein (APPSwe) under direction of the mouse prion protein promoter. Elevated levels of the AB1-42(43) peptide are detected in brain homogenates. By nine months of age, histological examination of brain tissue from these mice 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. |
| Molecular Note | The transgene is composed of a cDNA encoding a chimeric APP protein regulated by the mouse prion promoter. The chimeric APP molecule was created by replacing sequences encoding the Abeta domain of a 695 amino acid isoform of the murine sequence with the cognate sequences of the human gene (mutations K595N, M596L). The human mutations are found in familial Alzheimer's disease. Transgene expression was observed in the brain and heart by Western blot analysis using a monoclonal antibody recognizing the human Abeta region. |
| Mutations Made By | Dr. David Borchelt, University of Florida |
Tg(PSEN1dE9)S9Dbo
Allele Symbol: Tg(PSEN1dE9)S9Dbo
| Allele Name | transgene insertion S9, David R Borchelt |
|---|---|
| Allele Type | Transgenic (Humanized sequence, Inserted expressed sequence) |
| Allele Synonym(s) | PS1 deltaE9; PS1 transgene (line S-9); PS1-deltaE9; PS1dE9 transgene; PS1deltaE9 (line S-9); deltaE9; huPS1deltaE9; line S-9 |
| Gene Symbol and Name | Tg(PSEN1dE9)S9Dbo, transgene insertion S9, David R Borchelt |
| Gene Synonym(s) | PS1 deltaE9; PS1 transgene (line S-9); PS1-deltaE9; PS1dE9 transgene; PS1deltaE9 (line S-9); deltaE9; huPS1deltaE9; line S-9 |
| Promoter | Prnp, prion protein, mouse, laboratory |
| Expressed Gene | PSEN1, presenilin 1, human |
| Strain of Origin | (C57BL/6J x C3H/HeJ)F2 |
| Chromosome | UN |
| General Note | The deltaE9 PSEN1 protein variant fails to undergo endoproteolysis in cultured lymphoblasts from an affected human carrier and instead accumulates as the full-length, 40 kDa mutant protein (J:34323). Similarly, immunoblotting of of cortical and hippocampal extracts from transgenic mice under conditions that distinguish mouse and human full-length PSEN1 and their endoproteolytic derivatives demonstrates failure of the transgenic protein to undergo endoproteolysis. (J:104147) The amount of full-length mutant human PSEN1 in brains of deltaE9 PSEN1 transgenic mice exceeds by ~60% the cumulative amount of the full-length human PSEN1 and its N-terminal derivative in brains of transgenic mice expressing wild-type human PSEN1. (J:104147) |
| Molecular Note | The coding sequence of the transgene is derived from the cDNA of the familial Alzheimer disease- (FAD-) associated deltaE9 variant of human presenilin 1, which has a splice acceptor mutation upstream of exon 9 that results in a protein lacking amino acids 290-319. The mutant cDNA replaces the coding region of the mouse prion protein (Prp) gene in a construct that contains ~6 kb of genomic DNA upstream of the primary PRP translation start site and includes the noncoding first exon and first intron and, following the inserted PSEN1 sequence, ~3 kb of 3' untranslated sequence; this construct has been shown to drive expression in both neurons and glial cells of the central nervous system (CNS). |
| Mutations Made By | Dr. David Borchelt, University of Florida |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Neurobiology Research
- Alzheimer's Disease
- APP and PSEN1 mutants
- Presenilin mutants
- strains expressing mutant APP
- Behavioral and Learning Defects
- Alzheimer's Disease
Genotype: Tg(APP695)3Dbo related
- Neurobiology Research
- Alzheimer's Disease
- Neurodegeneration
Mammalian Phenotype Terms by Genotype
Genotype: Tg(APP695)3Dbo/0 Tg(PSEN1dE9)S9Dbo/0
B6.Cg-Tg(APP695)3Dbo Tg(PSEN1dE9)S9Dbo/Mmjax
nervous system phenotype
- amyloid beta deposits
- (MGI Ref ID J:157228)
homeostasis/metabolism phenotype
- amyloid beta deposits
- (MGI Ref ID J:157228)
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Tg(APP695)3Dbo/0 Tg(PSEN1dE9)S9Dbo/0
Not Specified
nervous system phenotype
- abnormal amacrine cell morphology
- distribution of amacrine cell processes is disrupted as determined by syntaxin 1 staining (MGI Ref ID J:139070)
- abnormal microglial cell morphology
- increase in microglial cell activity in retina is observed in 12-15 month old transgenics (MGI Ref ID J:139070)
- microglia density, but not cell body size, is increased in transgenics (MGI Ref ID J:139070)
- microglia processes in the retina are thicker and display a dendritic-like appearance as compared to control (MGI Ref ID J:139070)
- amyloid beta deposits
- 100% of females and 75% of males have plaques in retina by 15-16 months (MGI Ref ID J:139070)
- plaque size ranges from 5-20 um, larger plaques are observed at 15-16 months (MGI Ref ID J:139070)
- plaques appear earlier in females than in males and increase in number over time (MGI Ref ID J:139070)
- plaques have radial branches with a central core (MGI Ref ID J:139070)
- thioflavine-S positive plaques are observed in the retina beginning at 12 months of age (MGI Ref ID J:139070)
vision/eye phenotype
- abnormal amacrine cell morphology
- distribution of amacrine cell processes is disrupted as determined by syntaxin 1 staining (MGI Ref ID J:139070)
- abnormal eye electrophysiology
- abnormal retina morphology
- most plaques (34.7% and 41% respectively) are found in the inner and outer plexiform layers (MGI Ref ID J:139070)
- thickness of the retinal nuclear layers is similar to control, suggesting that there is no obvious neuronal cell loss (MGI Ref ID J:139070)
- thioflavine-S positive plaques are observed in the retina beginning at 12 months of age (MGI Ref ID J:139070)
- abnormal retinal inner plexiform layer morphology
- abnormal retinal outer plexiform layer morphology
immune system phenotype
- abnormal microglial cell morphology
- increase in microglial cell activity in retina is observed in 12-15 month old transgenics (MGI Ref ID J:139070)
- microglia density, but not cell body size, is increased in transgenics (MGI Ref ID J:139070)
- microglia processes in the retina are thicker and display a dendritic-like appearance as compared to control (MGI Ref ID J:139070)
hematopoietic system phenotype
- abnormal microglial cell morphology
- increase in microglial cell activity in retina is observed in 12-15 month old transgenics (MGI Ref ID J:139070)
- microglia density, but not cell body size, is increased in transgenics (MGI Ref ID J:139070)
- microglia processes in the retina are thicker and display a dendritic-like appearance as compared to control (MGI Ref ID J:139070)
homeostasis/metabolism phenotype
- amyloid beta deposits
- 100% of females and 75% of males have plaques in retina by 15-16 months (MGI Ref ID J:139070)
- plaque size ranges from 5-20 um, larger plaques are observed at 15-16 months (MGI Ref ID J:139070)
- plaques appear earlier in females than in males and increase in number over time (MGI Ref ID J:139070)
- plaques have radial branches with a central core (MGI Ref ID J:139070)
- thioflavine-S positive plaques are observed in the retina beginning at 12 months of age (MGI Ref ID J:139070)
Genotype: Tg(APP695)3Dbo/0 Tg(PSEN1dE9)S9Dbo/0
involves: 129S1/Sv * 129X1/SvJ * C3H/HeJ * C57BL/6J
behavior/neurological phenotype
- abnormal spatial learning
- mice travel shorter distance in open-field and show less activity or excursions into central area; mice remain near periphery of apparatus rather than entering open center of field (MGI Ref ID J:123534)
- abnormal spatial reference memory
- 16-18 month-old mice swim farther to find platform and spend less time in platform vicinity than controls (MGI Ref ID J:123534)
- behavior/neurological phenotype
- (MGI Ref ID J:123534)
nervous system phenotype
- amyloid beta deposits
- one month following neuron injection with virus expressing short hairpin RNA to silence Bace1, there is a 38% reduction in amyloid beta burden in hippocampus compared to uninjected hippocampus (MGI Ref ID J:123534)
homeostasis/metabolism phenotype
- amyloid beta deposits
- one month following neuron injection with virus expressing short hairpin RNA to silence Bace1, there is a 38% reduction in amyloid beta burden in hippocampus compared to uninjected hippocampus (MGI Ref ID J:123534)
- amyloidosis
- mice display amyloid beta aggregates at 12 and 20 months (MGI Ref ID J:123534)
Genotype: Tg(APP695)3Dbo/0 Tg(PSEN1dE9)S9Dbo/0
involves: C3H/HeJ * C57BL/6J
nervous system phenotype
- amyloid beta deposits
- 150% increase in amyloid beta peptide 42 (MGI Ref ID J:87691)
- at 7 months of age, mice exhibit amyloid plaques in the hippocampus and cortex (MGI Ref ID J:104236)
- develops diffuse, compact, birefringent congophilic plaques in cortex and hippocampus (MGI Ref ID J:87691)
- ratio of amyloid beta peptide 40:42 is 0.75:1 (MGI Ref ID J:87691)
homeostasis/metabolism phenotype
- amyloid beta deposits
- 150% increase in amyloid beta peptide 42 (MGI Ref ID J:87691)
- at 7 months of age, mice exhibit amyloid plaques in the hippocampus and cortex (MGI Ref ID J:104236)
- develops diffuse, compact, birefringent congophilic plaques in cortex and hippocampus (MGI Ref ID J:87691)
- ratio of amyloid beta peptide 40:42 is 0.75:1 (MGI Ref ID J:87691)
References
- Savonenko A; Xu GM; Melnikova T; Morton JL; Gonzales V; Wong MP; Price DL; Tang F; Markowska AL; Borchelt DR. 2005. Episodic-like memory deficits in the APPswe/PS1dE9 mouse model of Alzheimer's disease: relationships to beta-amyloid deposition and neurotransmitter abnormalities. Neurobiol Dis 18(3):602-17. PubMed: 15755686MGI: J:104236
Additional References
- Verret L; Jankowsky JL; Xu GM; Borchelt DR; Rampon C. 2007. Alzheimer's-type amyloidosis in transgenic mice impairs survival of newborn neurons derived from adult hippocampal neurogenesis. J Neurosci 27(25):6771-80. PubMed: 17581964MGI: J:122001
Additional - Tg(APP695)3Dbo related
- Bailey AR; Hou H; Obregon DF; Tian J; Zhu Y; Zou Q; Nikolic WV; Bengtson M; Mori T; Murphy T; Tan J. 2012. Aberrant T-lymphocyte development and function in mice overexpressing human soluble amyloid precursor protein-alpha: implications for autism. FASEB J 26(3):1040-51. PubMed: 22085641MGI: J:182808
- Bailey AR; Hou H; Song M; Obregon DF; Portis S; Barger S; Shytle D; Stock S; Mori T; Sanberg PG; Murphy T; Tan J. 2013. GFAP expression and social deficits in transgenic mice overexpressing human sAPPalpha. Glia 61(9):1556-69. PubMed: 23840007MGI: J:199441
- Boissonneault V; Plante I; Rivest S; Provost P. 2009. MicroRNA-298 and microRNA-328 regulate expression of mouse beta-amyloid precursor protein-converting enzyme 1. J Biol Chem 284(4):1971-81. PubMed: 18986979MGI: J:146980
- Borchelt DR; Davis J; Fischer M; Lee MK; Slunt HH; Ratovitsky T; Regard J; Copeland NG; Jenkins NA; Sisodia SS; Price DL. 1996. A vector for expressing foreign genes in the brains and hearts of transgenic mice. Genet Anal 13(6):159-63. PubMed: 9117892MGI: J:80782
- Borchelt DR; Ratovitski T; van Lare J; Lee MK; Gonzales V; Jenkins NA; Copeland NG; Price DL; Sisodia SS. 1997. Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins. Neuron 19(4):939-45. PubMed: 9354339MGI: J:43788
- Borchelt DR; Thinakaran G; Eckman CB; Lee MK; Davenport F; Ratovitsky T; Prada CM; Kim G; Seekins S; Yager D; Slunt HH; Wang R; Seeger M; Levey AI; Gandy SE; Copeland NG; Jenkins NA; Price DL; Younkin SG; Sisodia SS. 1996. Familial Alzheimer's disease-linked presenilin 1 variants elevate Abeta1-42/1-40 ratio in vitro and in vivo. Neuron 17(5):1005-13. PubMed: 8938131MGI: J:80882
- Cai D; Zhong M; Wang R; Netzer WJ; Shields D; Zheng H; Sisodia SS; Foster DA; Gorelick FS; Xu H; Greengard P. 2006. Phospholipase D1 corrects impaired betaAPP trafficking and neurite outgrowth in familial Alzheimer's disease-linked presenilin-1 mutant neurons. Proc Natl Acad Sci U S A 103(6):1936-40. PubMed: 16449385MGI: J:106075
- Cai 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: 22542680MGI: J:192436
- Dodson SE; Andersen OM; Karmali V; Fritz JJ; Cheng D; Peng J; Levey AI; Willnow TE; Lah JJ. 2008. Loss of LR11/SORLA enhances early pathology in a mouse model of amyloidosis: evidence for a proximal role in Alzheimer's disease. J Neurosci 28(48):12877-86. PubMed: 19036982MGI: J:142501
- Dolev I; Fogel H; Milshtein H; Berdichevsky Y; Lipstein N; Brose N; Gazit N; Slutsky I. 2013. Spike bursts increase amyloid-beta 40/42 ratio by inducing a presenilin-1 conformational change. Nat Neurosci 16(5):587-95. PubMed: 23563578MGI: J:197603
- El-Amouri SS; Zhu H; Yu J; Marr R; Verma IM; Kindy MS. 2008. Neprilysin: an enzyme candidate to slow the progression of Alzheimer's disease. Am J Pathol 172(5):1342-54. PubMed: 18403590MGI: J:134308
- Fernandez-Martos CM; King AE; Atkinson RA; Woodhouse A; Vickers JC. 2015. Neurofilament light gene deletion exacerbates amyloid, dystrophic neurite, and synaptic pathology in the APP/PS1 transgenic model of Alzheimer's disease. Neurobiol Aging 36(10):2757-67. PubMed: 26344875MGI: J:232249
- Filali M; Lalonde R. 2009. Age-related cognitive decline and nesting behavior in an APPswe/PS1 bigenic model of Alzheimer's disease. Brain Res 1292:93-9. PubMed: 19643098MGI: J:157207
- Filali M; Lalonde R; Rivest S. 2011. Subchronic memantine administration on spatial learning, exploratory activity, and nest-building in an APP/PS1 mouse model of Alzheimer's disease. Neuropharmacology 60(6):930-6. PubMed: 21281652MGI: J:178504
- Filali M; Lalonde R; Rivest S. 2008. Cognitive and non-cognitive behaviors in an APPswe/PS1 bigenic model of Alzheimer's disease. Genes Brain Behav 8(2):143-8. PubMed: 19077180MGI: J:142183
- Gao L; Chen X; Tang Y; Zhao J; Li Q; Fan X; Xu H; Yin ZQ. 2015. Neuroprotective effect of memantine on the retinal ganglion cells of APPswe/PS1DeltaE9 mice and its immunomodulatory mechanisms. Exp Eye Res 135:47-58. PubMed: 25912193MGI: J:230333
- Garcia-Alloza M; Dodwell SA; Meyer-Luehmann M; Hyman BT; Bacskai BJ. 2006. Plaque-derived oxidative stress mediates distorted neurite trajectories in the Alzheimer mouse model. J Neuropathol Exp Neurol 65(11):1082-9. PubMed: 17086105MGI: J:120918
- Gureviciene I; Ikonen S; Gurevicius K; Sarkaki A; van Groen T; Pussinen R; Ylinen A; Tanila H. 2004. Normal induction but accelerated decay of LTP in APP + PS1 transgenic mice. Neurobiol Dis 15(2):188-95. PubMed: 15006688MGI: J:128772
- Helft J; Manicassamy B; Guermonprez P; Hashimoto D; Silvin A; Agudo J; Brown BD; Schmolke M; Miller JC; Leboeuf M; Murphy KM; Garcia-Sastre A; Merad M. 2012. Cross-presenting CD103+ dendritic cells are protected from influenza virus infection. J Clin Invest 122(11):4037-47. PubMed: 23041628MGI: J:193561
- Horiuchi H; Parajuli B; Wang Y; Azuma YT; Mizuno T; Takeuchi H; Suzumura A. 2015. Interleukin-19 acts as a negative autocrine regulator of activated microglia. PLoS One 10(3):e0118640. PubMed: 25794104MGI: J:229575
- Huang HJ; Liang KC; Ke HC; Chang YY; Hsieh-Li HM. 2011. Long-term social isolation exacerbates the impairment of spatial working memory in APP/PS1 transgenic mice. Brain Res 1371:150-60. PubMed: 21114967MGI: J:170247
- Iivonen H; Nurminen L; Harri M; Tanila H; Puolivali J. 2003. Hypothermia in mice tested in Morris water maze. Behav Brain Res 141(2):207-13. PubMed: 12742257MGI: J:130974
- 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: 14645205MGI: J:87691
- Jankowsky JL; Melnikova T; Fadale DJ; Xu GM; Slunt HH; Gonzales V; Younkin LH; Younkin SG; Borchelt DR; Savonenko AV. 2005. Environmental enrichment mitigates cognitive deficits in a mouse model of Alzheimer's disease. J Neurosci 25(21):5217-24. PubMed: 15917461MGI: J:98541
- Jankowsky JL; Slunt HH; Gonzales V; Jenkins NA; Copeland NG; Borchelt DR. 2004. APP processing and amyloid deposition in mice haplo-insufficient for presenilin 1. Neurobiol Aging 25(7):885-92. PubMed: 15212842MGI: J:102351
- Joly S; Lamoureux S; Pernet V. 2017. Nonamyloidogenic processing of amyloid beta precursor protein is associated with retinal function improvement in aging male APPswe/PS1DeltaE9 mice. Neurobiol Aging 53:181-191. PubMed: 28262325MGI: J:243377
- Kalesnykas G; Roschier U; Puolivali J; Wang J; Miettinen R. 2005. The effect of aging on the subcellular distribution of estrogen receptor-alpha in the cholinergic neurons of transgenic and wild-type mice. Eur J Neurosci 21(5):1437-42. PubMed: 15813954MGI: J:101077
- Kamphuis W; Kooijman L; Orre M; Stassen O; Pekny M; Hol EM. 2015. GFAP and vimentin deficiency alters gene expression in astrocytes and microglia in wild-type mice and changes the transcriptional response of reactive glia in mouse model for Alzheimer's disease. Glia 63(6):1036-56. PubMed: 25731615MGI: J:221193
- Kanekiyo T; Cirrito JR; Liu CC; Shinohara M; Li J; Schuler DR; Shinohara M; Holtzman DM; Bu G. 2013. Neuronal clearance of amyloid-beta by endocytic receptor LRP1. J Neurosci 33(49):19276-83. PubMed: 24305823MGI: J:204149
- Kanekiyo T; Liu CC; Shinohara M; Li J; Bu G. 2012. LRP1 in brain vascular smooth muscle cells mediates local clearance of Alzheimer's amyloid-beta. J Neurosci 32(46):16458-65. PubMed: 23152628MGI: J:192453
- Ke HC; Huang HJ; Liang KC; Hsieh-Li HM. 2011. Selective improvement of cognitive function in adult and aged APP/PS1 transgenic mice by continuous non-shock treadmill exercise. Brain Res 1403:1-11. PubMed: 21689809MGI: J:174067
- Khan UA; Liu L; Provenzano FA; Berman DE; Profaci CP; Sloan R; Mayeux R; Duff KE; Small SA. 2014. Molecular drivers and cortical spread of lateral entorhinal cortex dysfunction in preclinical Alzheimer's disease. Nat Neurosci 17(2):304-11. PubMed: 24362760MGI: J:208008
- Laird FM; Cai H; Savonenko AV; Farah MH; He K; Melnikova T; Wen H; Chiang HC; Xu G; Koliatsos VE; Borchelt DR; Price DL; Lee HK; Wong PC. 2005. BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. J Neurosci 25(50):11693-709. PubMed: 16354928MGI: J:123534
- Lazarov O; Morfini GA; Pigino G; Gadadhar A; Chen X; Robinson J; Ho H; Brady ST; Sisodia SS. 2007. Impairments in fast axonal transport and motor neuron deficits in transgenic mice expressing familial Alzheimer's disease-linked mutant presenilin 1. J Neurosci 27(26):7011-20. PubMed: 17596450MGI: J:122975
- Lee GD; Aruna JH; Barrett PM; Lei DL; Ingram DK; Mouton PR. 2005. Stereological analysis of microvascular parameters in a double transgenic model of Alzheimer's disease. Brain Res Bull 65(4):317-22. PubMed: 15811597MGI: J:135436
- Lesuisse C; Xu G; Anderson J; Wong M; Jankowsky J; Holtz G; Gonzalez V; Wong PC; Price DL; Tang F; Wagner S; Borchelt DR. 2001. Hyper-expression of human apolipoprotein E4 in astroglia and neurons does not enhance amyloid deposition in transgenic mice. Hum Mol Genet 10(22):2525-37. PubMed: 11709540MGI: J:72987
- Li G; Zou L; Jack CR Jr; Yang Y; Yang ES. 2007. Neuroprotective effect of Coenzyme Q10 on ischemic hemisphere in aged mice with mutations in the amyloid precursor protein. Neurobiol Aging 28(6):877-82. PubMed: 16806588MGI: J:121939
- Li L; Zhang X; Yang D; Luo G; Chen S; Le W. 2009. Hypoxia increases Abeta generation by altering beta- and gamma-cleavage of APP. Neurobiol Aging 30(7):1091-8. PubMed: 18063223MGI: J:152965
- Li Q; Navakkode S; Rothkegel M; Soong TW; Sajikumar S; Korte M. 2017. Metaplasticity mechanisms restore plasticity and associativity in an animal model of Alzheimer's disease. Proc Natl Acad Sci U S A 114(21):5527-5532. PubMed: 28484012MGI: J:242199
- Liang C; Zhu H; Xu Y; Huang L; Ma C; Deng W; Liu Y; Qin C. 2012. MicroRNA-153 negatively regulates the expression of amyloid precursor protein and amyloid precursor-like protein 2. Brain Res 1455:103-13. PubMed: 22510281MGI: J:186457
- Liu L; Ikonen S; Heikkinen T; Heikkila M; Puolivali J; van Groen T; Tanila H. 2002. Effects of fimbria-fornix lesion and amyloid pathology on spatial learning and memory in transgenic APP+PS1 mice. Behav Brain Res 134(1-2):433-45. PubMed: 12191831MGI: J:129807
- Liu L; Tapiola T; Herukka SK; Heikkila M; Tanila H. 2003. Abeta levels in serum, CSF and brain, and cognitive deficits in APP + PS1 transgenic mice. Neuroreport 14(1):163-6. PubMed: 12544850MGI: J:89843
- Liu Y; Yoo MJ; Savonenko A; Stirling W; Price DL; Borchelt DR; Mamounas L; Lyons WE; Blue ME; Lee MK. 2008. Amyloid pathology is associated with progressive monoaminergic neurodegeneration in a transgenic mouse model of Alzheimer's disease. J Neurosci 28(51):13805-14. PubMed: 19091971MGI: J:143521
- Lopez JR; Lyckman A; Oddo S; Laferla FM; Querfurth HW; Shtifman A. 2008. Increased intraneuronal resting [Ca2+] in adult Alzheimer's disease mice. J Neurochem 105(1):262-71. PubMed: 18021291MGI: J:141555
- Luo H; Wu Q; Ye X; Xiong Y; Zhu J; Xu J; Diao Y; Zhang D; Wang M; Qiu J; Miao J; Zhang W; Wan J. 2014. Genome-wide analysis of miRNA signature in the APPswe/PS1DeltaE9 mouse model of alzheimer's disease. PLoS One 9(8):e101725. PubMed: 25148207MGI: J:221085
- Manczak M; Reddy PH. 2012. Abnormal interaction between the mitochondrial fission protein Drp1 and hyperphosphorylated tau in Alzheimer's disease neurons: implications for mitochondrial dysfunction and neuronal damage. Hum Mol Genet 21(11):2538-47. PubMed: 22367970MGI: J:183771
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