JAX
Mouse Strain Datasheet
B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
Also Known As: 5XFAD
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. These 5XFAD transgenic mice rapidly recapitulate major features of Alzheimer's Disease amyloid pathology and may be useful models of intraneuronal Aβ-42 induced neurodegeneration and amyloid plaque formation.
Donating Investigator
IMR Colony, The Jackson Laboratory
Genetic overview
| Genetic Background | Generation |
|---|---|
|
N6+N1F5
|
Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas
| Allele Type |
|---|
| Transgenic (Humanized sequence, Inserted expressed sequence) |
Detailed Description
Hemizygous mice are viable and fertile. These 5XFAD transgenic mice overexpress both mutant human APP(695) with the Swedish (K670N, M671L), Florida (I716V), and London (V717I) Familial Alzheimer's Disease (FAD) mutations and human PS1 harboring two FAD mutations, M146L and L286V. Expression of both transgenes is regulated by neural-specific elements of the mouse Thy1 promoter to drive overexpression in the brain. Mice from this founder line have high APP expression correlating with high burden and accelerated accumulation of the 42 amino acid species of beta-amyloid (Aβ-42). 5XFAD mice generate Aβ-42 almost exclusively and rapidly accumulate massive cerebral levels. On the B6SJL F1 genetic background (see MMRRC stock 34840), intraneuronal Abeta;-42 accumulation is observed starting at 1.5 months of age, just prior to amyloid deposition and gliosis, which begins at two months of age. On a congenic C57BL/6J genetic background (see MMRRC stock 34848) it has been the observation of the MMRRC that this phenotype is not as robust as that demonstrated in the B6SJL hybrid background (view data). In addition, these mice have reduced synaptic marker protein levels, increased p25 levels, neuron loss, and memory impairment in the Y-maze test. 5XFAD transgenic mice rapidly recapitulate major features of Alzheimer's Disease amyloid pathology and may be useful models of intraneuronal Aβ-42 induced neurodegeneration and amyloid plaque formation.
This strain does not carry the retinal degeneration allele Pde6brd1.
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. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
Development
A transgene was designed with a mutant human amyloid beta (A4) precursor protein (APP) cDNA sequence (altered to include the APP K670N/M671L (Swedish) + I716V (Florida) + V717I (London) Familial Alzheimer's Disease (FAD) mutations) inserted into exon 2 of the mouse Thy1 gene. A second transgene was designed with a mutant human presenilin 1 (Alzheimer disease 3) (PSEN1 or PS1) cDNA sequence (altered to include the PS1 M146L + L286V FAD mutations) inserted into exon 2 of the mouse Thy1 gene. Both transgenes were added together in equal proportions and co-injected into the pronuclei of single-cell "C57/B6XSJL" hybrid embryos. Founders from the highest APP expressing line (Tg6799) were bred with (B6/SJL)F1 for more than 10 generations with stable germ-line transmission and expression of both transgenes, demonstrating that these "5XFAD" mice breed as single transgenics. The mice were then backcrossed to C57BL/6J mice using a speed congenic protocol and the retinal degeneration allele Pde6brd1 was bred out of the strain. Of note, the APP transgene includes the 5' untranslated region and thus contains a putative interleukin-1beta translational enhancer element.
Expression Data
| Expressed Gene | APP695, amyloid beta (A4) precursor protein (chimeric), mouse/human chimera |
|---|---|
| Expressed Gene | PSEN1, presenilin 1, human |
| Site of Expression |
Control Suggestions
Selected References
- Oakley H; Cole SL; Logan S; Maus E; Shao P; Craft J; Guillozet-Bongaarts A; Ohno M; Disterhoft J; Van Eldik L; Berry R; Vassar R. 2006. Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. J Neurosci 26(40):10129-40. PubMed: 17021169MGI: J:112949
Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas
Allele Symbol: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas
| Allele Name | transgene insertion 6799, Robert Vassar |
|---|---|
| Allele Type | Transgenic (Humanized sequence, Inserted expressed sequence) |
| Allele Synonym(s) | 5XFAD; 5XFAD APP/PS1; 5XFAD line Tg6799; Tg(APP*Swe*Fl*Lon,PSEN1*M146L*L286V)6799Vas; Tg-5xFAD; Tg6799 |
| Gene Symbol and Name | Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas, transgene insertion 6799, Robert Vassar |
| Gene Synonym(s) | 5XFAD; 5XFAD line Tg6799; Tg6799 |
| Promoter | Thy1, thymus cell antigen 1, theta, mouse, laboratory |
| Expressed Gene | APP695, amyloid beta (A4) precursor protein (chimeric), mouse/human chimera |
| Expressed Gene | PSEN1, presenilin 1, human |
| Strain of Origin | (C57BL/6 x SJL)F1 |
| Chromosome | UN |
| General Note | Three transgenic lines coexpressing the APP and PSEN1 proteins at high, medium and low levels, respectively designated Tg6799, Tg7031, and Tg7092, were propagated for analysis, most of which employed Tg6799. Phenotypic Similarity to Human Syndrome: Macular Degeneration, Age-Related J:214858. |
| Molecular Note | Four familial Alzheimer disease- (FAD-) associated mutations were introduced into a single human amyloid precursor protein cDNA: the "Swedish" double mutation (K670N/M671L); the "Florida" mutation (I716V); and the "London" mutation (V717I). Two FAD-associated mutations, M146L and L286V, likewise were introduced into a human presenilin 1 cDNA. Each cDNA was then cloned independently into the mouse thymus cell antigen 1 gene, replacing a segment that contains thymus-specific elements so that expression of the transgenes is targeted only to the brain. Equal molar amounts of the two transgenes were coinjected into pronuclei of single-celled embryos. |
| Mutations Made By | Robert Vassar, Northwestern University |
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
- Neurodegeneration
- Alzheimer's Disease
- Research Tools
- Neurobiology Research
Mammalian Phenotype Terms by Genotype
Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0
B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas
behavior/neurological phenotype
- decreased anxiety-related response
- increased open to total arm entry ratio in 5 month old females, however, phenotype is more severe in homozygotes (MGI Ref ID J:229382)
- limb grasping
- increased clasping during tail suspension in 5 month old females as compared to controls, however clasping in homozygotes is more severe (MGI Ref ID J:229382)
growth/size/body region phenotype
- decreased body weight
- reduced body weight at 2 months old females, but weight is similar to control by 5 months of age (MGI Ref ID J:229382)
Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas
B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas
behavior/neurological phenotype
- abnormal posture
- postural abnormalities observed in 9 month old males (MGI Ref ID J:229382)
- abnormal spatial reference memory
- impaired spacial reference memory in 5 month old females (MGI Ref ID J:229382)
- decreased anxiety-related response
- impaired balance
- 9 month old males either remain still on balance beam or fall off due to hind limb paresis (MGI Ref ID J:229382)
- impairment in balance and general motor coordination in 5 month old females as measured by the balance beam (MGI Ref ID J:229382)
- poor performance in string suspension paradigm as compared to wild-type and female hemizygotes at 5 months of age (MGI Ref ID J:229382)
- impaired coordination
- impairment in balance and general motor coordination in 5 month old females as measured by the balance beam (MGI Ref ID J:229382)
- impaired spatial learning
- impaired acquisition in 2 and 5 month old females; escape latencies increase over 5 days of training (MGI Ref ID J:229382)
- impaired swimming
- decreased average swimming speed during cued training in 5 month old females, however no difference in day 3 escape latency (MGI Ref ID J:229382)
- limb grasping
- increased clasping behavior during tail suspension in 5 month old females (MGI Ref ID J:229382)
- paresis
- hind limb paresis in 9 month old males (MGI Ref ID J:229382)
- pup cannibalization
- in females older than 5 months of age (MGI Ref ID J:229382)
growth/size/body region phenotype
- cachexia
- wasting observed in 9 month old males (MGI Ref ID J:229382)
- decreased body weight
- reduced body weight in 2 and 5 month old females (MGI Ref ID J:229382)
homeostasis/metabolism phenotype
- amyloid beta deposits
- increase in plaque load in spinal cord of 9 month old males (MGI Ref ID J:229382)
- increased SDS-soluble Abeta1-42 levels at 2 and 5 months (females) as compared to hemizygotes (MGI Ref ID J:229382)
- increased TBS-soluble Abeta1-42 and Abeta1-40 levels at 2 and 5 months (females) as compared to hemizygotes (MGI Ref ID J:229382)
- increased extracellular plaque load and intracellular Abeta immunoreacitivy in large spinal cord neurons in 9 month old males (MGI Ref ID J:229382)
- increased plaque load in cortex, hippocampus and thalamus at 2 (females), 5 (females) and 9 (males) months (MGI Ref ID J:229382)
nervous system phenotype
- amyloid beta deposits
- increase in plaque load in spinal cord of 9 month old males (MGI Ref ID J:229382)
- increased SDS-soluble Abeta1-42 levels at 2 and 5 months (females) as compared to hemizygotes (MGI Ref ID J:229382)
- increased TBS-soluble Abeta1-42 and Abeta1-40 levels at 2 and 5 months (females) as compared to hemizygotes (MGI Ref ID J:229382)
- increased extracellular plaque load and intracellular Abeta immunoreacitivy in large spinal cord neurons in 9 month old males (MGI Ref ID J:229382)
- increased plaque load in cortex, hippocampus and thalamus at 2 (females), 5 (females) and 9 (males) months (MGI Ref ID J:229382)
- axonal spheroids
- increase in axonal swellings in pons and gray matter of spinal cord of 9 month old male homozygotes as compared to hemizygotes (MGI Ref ID J:229382)
reproductive system phenotype
- decreased litter size
- in females older than 5 months of age (MGI Ref ID J:229382)
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0
involves: C57BL/6 * SJL
behavior/neurological phenotype
- abnormal spatial learning
- by 4-5 months of age, defects in Y-maze alternation are detected in transgenic mice, indicating impaired spatial learning/memory (MGI Ref ID J:112949)
nervous system phenotype
- abnormal hippocampus morphology
- cortical layer 1 is significantly thinner than in control brains (MGI Ref ID J:112949)
- abnormal neuron morphology
- some neurons contain intraneuronal aggregates and display disrupted morphology (MGI Ref ID J:112949)
- abnormal subiculum morphology
- neurons in subiculum are very pale, or absent (MGI Ref ID J:112949)
- amyloid beta deposits
- amyloid deposition increases rapidly with increasing age (MGI Ref ID J:112949)
- mice show Abeta42 deposits at 2 months of age; Abeta40 levels are lower in amyloid deposits; mice show robust intraneuronal amyloid deposition (MGI Ref ID J:112949)
- plaques appear first in deep cortical layers and in subiculum, and spread with age to fill most of cortex, subiculum and hippocampus; also, less numerous deposits are observed in thalamus, brainstem and olfactory bulb in older mice (MGI Ref ID J:112949)
- astrocytosis
- (MGI Ref ID J:112949)
- brain inflammation
- transgenic mice display neuroinflammation (MGI Ref ID J:112949)
- decreased cerebral cortex pyramidal cell number
- large neurons in cortical layer 5 are reduced in number (MGI Ref ID J:112949)
- gliosis
- microgliosis and astrogliosis is seen in plaque-bearing regions of the brain by 2 months of age; numbers of activated astrocytes and microglia increases with age (MGI Ref ID J:112949)
- neurodegeneration
- synapse degeneration begins at 4 months of age, compared to nontransgenic controls, as shown by reduction in levels of synaptic markers; neurodeneration marker p25 level is ~150% of control at 9 and 12 months (MGI Ref ID J:112949)
immune system phenotype
- brain inflammation
- transgenic mice display neuroinflammation (MGI Ref ID J:112949)
homeostasis/metabolism phenotype
- amyloid beta deposits
- amyloid deposition increases rapidly with increasing age (MGI Ref ID J:112949)
- mice show Abeta42 deposits at 2 months of age; Abeta40 levels are lower in amyloid deposits; mice show robust intraneuronal amyloid deposition (MGI Ref ID J:112949)
- plaques appear first in deep cortical layers and in subiculum, and spread with age to fill most of cortex, subiculum and hippocampus; also, less numerous deposits are observed in thalamus, brainstem and olfactory bulb in older mice (MGI Ref ID J:112949)
Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0
B6SJL-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax
homeostasis/metabolism phenotype
- amyloid beta deposits
- retinal amyloid beta accumulates in the retinal pigment epithelial (RPE) layer and amyloid beta deposits are seen beneath the RPE layer (MGI Ref ID J:214858)
nervous system phenotype
- amyloid beta deposits
- retinal amyloid beta accumulates in the retinal pigment epithelial (RPE) layer and amyloid beta deposits are seen beneath the RPE layer (MGI Ref ID J:214858)
pigmentation phenotype
- abnormal retinal pigment epithelium morphology
- abundant intracellular amyloid beta is seen in the cytosol of RPE and with increasing intracellular accumulation of amyloid beta, tight junction integrity is attenuated and disorganized (MGI Ref ID J:214858)
- abnormal retinal pigmentation
- 12 month old mutants show hypopigmentation in the RPE layer (MGI Ref ID J:214858)
vision/eye phenotype
- abnormal Bruch membrane morphology
- thickened Bruch membrane is seen in the retina of 12 month old mutants (MGI Ref ID J:214858)
- abnormal eye morphology
- drusen-like deposit is seen between the retinal pigment epithelium (RPE) layer and Bruch membrane in 12 month old mutants (MGI Ref ID J:214858)
- abnormal retina morphology
- large vacuoles are seen in the retina of 12 month old mutants (MGI Ref ID J:214858)
- abnormal retinal pigment epithelium morphology
- abundant intracellular amyloid beta is seen in the cytosol of RPE and with increasing intracellular accumulation of amyloid beta, tight junction integrity is attenuated and disorganized (MGI Ref ID J:214858)
- abnormal retinal pigmentation
- 12 month old mutants show hypopigmentation in the RPE layer (MGI Ref ID J:214858)
Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/0
involves: C57BL/6 * C57BL/6J * CBA * SJL
mortality/aging
- premature death
- decreased survival at 10 months of age (MGI Ref ID J:201809)
nervous system phenotype
- amyloid beta deposits
- (MGI Ref ID J:201809)
homeostasis/metabolism phenotype
- amyloid beta deposits
- (MGI Ref ID J:201809)
Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/?
involves: C57BL/6 * SJL
behavior/neurological phenotype
- abnormal response to novel object
- poor novel object recognition (MGI Ref ID J:208030)
- impaired contextual conditioning behavior
- decreased % of time freezing in contextual fear conditioning test (MGI Ref ID J:208030)
- impaired cued conditioning behavior
- decreased % of time freezing in cued fear conditioning test (MGI Ref ID J:208030)
hematopoietic system phenotype
- abnormal microglial cell activation
- increased percentage of activated microglia as compared to controls (MGI Ref ID J:208030)
immune system phenotype
- abnormal microglial cell activation
- increased percentage of activated microglia as compared to controls (MGI Ref ID J:208030)
nervous system phenotype
- abnormal astrocyte physiology
- increased percentage of reactive astrocytes as compared to controls (MGI Ref ID J:208030)
- abnormal long term depression
- decreased magnitude of long term depression as compared to controls (MGI Ref ID J:208030)
- abnormal microglial cell activation
- increased percentage of activated microglia as compared to controls (MGI Ref ID J:208030)
- amyloid beta deposits
homeostasis/metabolism phenotype
Genotype: Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/?
involves: 129S4/SvJae * C57BL/6 * SJL
References
- Oakley H; Cole SL; Logan S; Maus E; Shao P; Craft J; Guillozet-Bongaarts A; Ohno M; Disterhoft J; Van Eldik L; Berry R; Vassar R. 2006. Intraneuronal beta-amyloid aggregates, neurodegeneration, and neuron loss in transgenic mice with five familial Alzheimer's disease mutations: potential factors in amyloid plaque formation. J Neurosci 26(40):10129-40. PubMed: 17021169MGI: J:112949
Additional - Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas related
- Ahn HJ; Glickman JF; Poon KL; Zamolodchikov D; Jno-Charles OC; Norris EH; Strickland S. 2014. A novel Abeta-fibrinogen interaction inhibitor rescues altered thrombosis and cognitive decline in Alzheimer's disease mice. J Exp Med 211(6):1049-62. PubMed: 24821909MGI: J:213119
- Annunziata I; Patterson A; Helton D; Hu H; Moshiach S; Gomero E; Nixon R; d'Azzo A. 2013. Lysosomal NEU1 deficiency affects amyloid precursor protein levels and amyloid-beta secretion via deregulated lysosomal exocytosis. Nat Commun 4:2734. PubMed: 24225533MGI: J:223503
- Avrahami L; Farfara D; Shaham-Kol M; Vassar R; Frenkel D; Eldar-Finkelman H. 2013. Inhibition of glycogen synthase kinase-3 ameliorates beta-amyloid pathology and restores lysosomal acidification and mammalian target of rapamycin activity in the Alzheimer disease mouse model: in vivo and in vitro studies. J Biol Chem 288(2):1295-306. PubMed: 23155049MGI: J:193739
- Aytan N; Choi JK; Carreras I; Kowall NW; Jenkins BG; Dedeoglu A. 2013. Combination therapy in a transgenic model of Alzheimer's disease. Exp Neurol 250:228-38. PubMed: 24120437MGI: J:206610
- Baik SH; Cha MY; Hyun YM; Cho H; Hamza B; Kim DK; Han SH; Choi H; Kim KH; Moon M; Lee J; Kim M; Irimia D; Mook-Jung I. 2014. Migration of neutrophils targeting amyloid plaques in Alzheimer's disease mouse model. Neurobiol Aging 35(6):1286-92. PubMed: 24485508MGI: J:213882
- Baik SH; Kang S; Son SM; Mook-Jung I. 2016. Microglia contributes to plaque growth by cell death due to uptake of amyloid beta in the brain of Alzheimer's disease mouse model. Glia 64(12):2274-2290. PubMed: 27658617MGI: J:236228
- Baruch K; Deczkowska A; Rosenzweig N; Tsitsou-Kampeli A; Sharif AM; Matcovitch-Natan O; Kertser A; David E; Amit I; Schwartz M. 2016. PD-1 immune checkpoint blockade reduces pathology and improves memory in mouse models of Alzheimer's disease. Nat Med 22(2):135-7. PubMed: 26779813MGI: J:233342
- Baruch K; Kertser A; Porat Z; Schwartz M. 2015. Cerebral nitric oxide represses choroid plexus NFkappaB-dependent gateway activity for leukocyte trafficking. EMBO J 34(13):1816-28. PubMed: 25940071MGI: J:222768
- Baruch K; Rosenzweig N; Kertser A; Deczkowska A; Sharif AM; Spinrad A; Tsitsou-Kampeli A; Sarel A; Cahalon L; Schwartz M. 2015. Breaking immune tolerance by targeting Foxp3(+) regulatory T cells mitigates Alzheimer's disease pathology. Nat Commun 6:7967. PubMed: 26284939MGI: J:224985
- Beck SJ; Guo L; Phensy A; Tian J; Wang L; Tandon N; Gauba E; Lu L; Pascual JM; Kroener S; Du H. 2016. Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer's disease. Nat Commun 7:11483. PubMed: 27151236MGI: J:239938
- Bhattacharya S; Haertel C; Maelicke A; Montag D. 2014. Galantamine slows down plaque formation and behavioral decline in the 5XFAD mouse model of Alzheimer's disease. PLoS One 9(2):e89454. PubMed: 24586789MGI: J:213824
- Brower CS; Piatkov KI; Varshavsky A. 2013. Neurodegeneration-associated protein fragments as short-lived substrates of the N-end rule pathway. Mol Cell 50(2):161-71. PubMed: 23499006MGI: J:198127
- Bundy JL; Vied C; Nowakowski RS. 2017. Sex differences in the molecular signature of the developing mouse hippocampus. BMC Genomics 18(1):237. PubMed: 28302071MGI: J:241867
- Burgert T; Schmidt V; Caglayan S; Lin F; Fuchtbauer A; Fuchtbauer EM; Nykjaer A; Carlo AS; Willnow TE. 2013. SORLA-dependent and -independent functions for PACS1 in control of amyloidogenic processes. Mol Cell Biol 33(21):4308-20. PubMed: 24001769MGI: J:205418
- Buskila Y; Crowe SE; Ellis-Davies GC. 2013. Synaptic deficits in layer 5 neurons precede overt structural decay in 5xFAD mice. Neuroscience 254:152-9. PubMed: 24055684MGI: J:207428
- Cacciottolo M; Christensen A; Moser A; Liu J; Pike CJ; Smith C; LaDu MJ; Sullivan PM; Morgan TE; Dolzhenko E; Charidimou A; Wahlund LO; Wiberg MK; Shams S; Chiang GC; Finch CE. 2016. The APOE4 allele shows opposite sex bias in microbleeds and Alzheimer's disease of humans and mice. Neurobiol Aging 37:47-57. PubMed: 26686669MGI: J:234434
- 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
- Carlo AS; Gustafsen C; Mastrobuoni G; Nielsen MS; Burgert T; Hartl D; Rohe M; Nykjaer A; Herz J; Heeren J; Kempa S; Petersen CM; Willnow TE. 2013. The pro-neurotrophin receptor sortilin is a major neuronal apolipoprotein E receptor for catabolism of amyloid-beta peptide in the brain. J Neurosci 33(1):358-70. PubMed: 23283348MGI: J:193915
- Cha MY; Cho HJ; Kim C; Jung YO; Kang MJ; Murray ME; Hong HS; Choi YJ; Choi H; Kim DK; Choi H; Kim J; Dickson DW; Song HK; Cho JW; Yi EC; Kim J; Jin SM; Mook-Jung I. 2015. Mitochondrial ATP synthase activity is impaired by suppressed O-GlcNAcylation in Alzheimer's disease. Hum Mol Genet 24(22):6492-504. PubMed: 26358770MGI: J:226496
- Chen R; Zhang J; Wu Y; Wang D; Feng G; Tang YP; Teng Z; Chen C. 2012. Monoacylglycerol lipase is a therapeutic target for Alzheimer's disease. Cell Rep 2(5):1329-39. PubMed: 23122958MGI: J:196345
- Cho WH; Park JC; Chung C; Jeon WK; Han JS. 2014. Learning strategy preference of 5XFAD transgenic mice depends on the sequence of place/spatial and cued training in the water maze task. Behav Brain Res 273:116-22. PubMed: 25078295MGI: J:217100
- Cho WH; Park JC; Kim DH; Kim MS; Lee SY; Park H; Kang JH; Yeon SW; Han JS. 2014. ID1201, the ethanolic extract of the fruit of Melia toosendan ameliorates impairments in spatial learning and reduces levels of amyloid beta in 5XFAD mice. Neurosci Lett 583:170-5. PubMed: 25281546MGI: J:218544
- Christensen DZ; Bayer TA; Wirths O. 2009. Formic acid is essential for immunohistochemical detection of aggregated intraneuronal Abeta peptides in mouse models of Alzheimer's disease. Brain Res 1301:116-25. PubMed: 19751708MGI: J:158791
- Corbett GT; Gonzalez FJ; Pahan K. 2015. Activation of peroxisome proliferator-activated receptor alpha stimulates ADAM10-mediated proteolysis of APP. Proc Natl Acad Sci U S A 112(27):8445-50. PubMed: 26080426MGI: J:223748
- Cortes-Canteli M; Paul J; Norris EH; Bronstein R; Ahn HJ; Zamolodchikov D; Bhuvanendran S; Fenz KM; Strickland S. 2010. Fibrinogen and beta-amyloid association alters thrombosis and fibrinolysis: a possible contributing factor to Alzheimer's disease. Neuron 66(5):695-709. PubMed: 20547128MGI: J:167873
- Crouzin N; Baranger K; Cavalier M; Marchalant Y; Cohen-Solal C; Roman FS; Khrestchatisky M; Rivera S; Feron F; Vignes M. 2013. Area-specific alterations of synaptic plasticity in the 5XFAD mouse model of Alzheimer's disease: dissociation between somatosensory cortex and hippocampus. PLoS One 8(9):e74667. PubMed: 24069328MGI: J:206029
- Crowe SE; Ellis-Davies GC. 2014. Spine pruning in 5xFAD mice starts on basal dendrites of layer 5 pyramidal neurons. Brain Struct Funct 219(2):571-80. PubMed: 23417057MGI: J:214142
- Crowe SE; Ellis-Davies GC. 2013. In vivo characterization of a bigenic fluorescent mouse model of Alzheimer's disease with neurodegeneration. J Comp Neurol 521(10):Spc1. PubMed: 23605442MGI: J:200729
- Cui Y; Huang M; He Y; Zhang S; Luo Y. 2011. Genetic Ablation of Apolipoprotein A-IV Accelerates Alzheimer's Disease Pathogenesis in a Mouse Model. Am J Pathol 178(3):1298-308. PubMed: 21356380MGI: J:169682
- Devi L; Ohno M. 2013. Deletion of the eIF2alpha Kinase GCN2 fails to rescue the memory decline associated with Alzheimer's disease. PLoS One 8(10):e77335. PubMed: 24146979MGI: J:209106
- Devi L; Ohno M. 2015. Effects of BACE1 haploinsufficiency on APP processing and Abeta concentrations in male and female 5XFAD Alzheimer mice at different disease stages. Neuroscience 307:128-37. PubMed: 26314636MGI: J:227527
- Devi L; Ohno M. 2010. Genetic reductions of beta-site amyloid precursor protein-cleaving enzyme 1 and amyloid-beta ameliorate impairment of conditioned taste aversion memory in 5XFAD Alzheimer's disease model mice. Eur J Neurosci 31(1):110-8. PubMed: 20092558MGI: J:158363
- Devi L; Ohno M. 2010. Phospho-eIF2alpha level is important for determining abilities of BACE1 reduction to rescue cholinergic neurodegeneration and memory defects in 5XFAD mice. PLoS One 5(9):e12974. PubMed: 20886088MGI: J:165103
- Devi L; Ohno M. 2014. PERK mediates eIF2alpha phosphorylation responsible for BACE1 elevation, CREB dysfunction and neurodegeneration in a mouse model of Alzheimer's disease. Neurobiol Aging 35(10):2272-81. PubMed: 24889041MGI: J:218077
- Devi L; Ohno M. 2012. Mitochondrial dysfunction and accumulation of the beta-secretase-cleaved C-terminal fragment of APP in Alzheimer's disease transgenic mice. Neurobiol Dis 45(1):417-24. PubMed: 21933711MGI: J:179837
- Dinkins MB; Dasgupta S; Wang G; Zhu G; Bieberich E. 2014. Exosome reduction in vivo is associated with lower amyloid plaque load in the 5XFAD mouse model of Alzheimer's disease. Neurobiol Aging 35(8):1792-800. PubMed: 24650793MGI: J:214860
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