JAX
Mouse Strain Datasheet - 008169
B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J
The PS19 mouse model harbors the T34 isoform of microtubule-associated protein tau with one N-terminal insert and four microtubule binding repeats (1N4R) encoding the human P301S mutation, all driven by the mouse prion protein promoter. These mice are useful in studying neurofibrillary tangles, neurodegenerative tauopathy and Alzheimer's disease.
Donating Investigator
Virginia M Lee, University of Pennsylvania
Genetic overview
| Genetic Background | Generation |
|---|---|
|
?+N3F1
|
Tg(Prnp-MAPT*P301S)PS19Vle
| Allele Type |
|---|
| Transgenic (Humanized sequence, Inserted expressed sequence) |
Base Price
Starting at:
| $255.00 Domestic price for female |
| $329.00 Domestic price for breeder pair |
Detailed Description
These PS19 transgenic mice (P301S Tg mice) express the P301S mutant form of human microtubule-associated protein tau (MAPT), under the direction of the mouse prion protein promoter (Prnp). The expression of the mutant human MAPT is five-fold higher than the expression of the endogenous mouse MAPT protein. Hyperphosphorylated, insoluble mutant human MAPT protein in the brain accumulates with age causing decreased microtubule binding/density. At three months of age, transgenic mice exhibit clasping and limb retraction when lifted by the tail, which progresses to limb weakness. By ten months of age the mice exhibit a hunched back and paralysis, followed by inability to feed. Transgenic mice have a median lifespan of approximately nine months with approximately 80% dying by 12 months. Histological analysis reveals neuron degeneration in hippocampus and ventricular dilatation (brain atrophy) by eight months of age, although significant neuron degeneration in the hippocampus occurs at approximately nine months of age. Neuron loss spreads to the amygdala, neocortex and entorhinal cortex by 12 months of age. Defective translocation of endoplasmic reticulum proteins in affected neurons is observed as early as three months of age. The onset of neurofibrillay tangle formation in the neocortex, amygdala, hippocampus, brain stem and spinal cord is five months of age. Transgenic mice display neuroinflammation with microglial activation and astrogliosis. The ultrastructure of the neurofibrillay tangle-like lesions detected is similar to that found in brain lesions of human Alzheimer's disease and tauopathy patients. Degradation of synaptic function is significant by six months of age. These mice cannot be bred to homozygosity as homozygous females do not mate.
Researchers should note that these mice may harbor a Pde6brd1 allele. In animals that are homozygous for this allele, retinal degeneration is observed by 3-4 weeks of age. We are currently in the process of removing the Pde6brd1 mutation from our colony (May 2017).
The phenotype of PS19 transgenic mice described above is based on the published information available as of 2008. In 2012-2013, publications using PS19 mice on a B6C3F1 or B6C3 genetic background report attenuated formation of tau pathology (hyperphosphorylated tau inclusions prominent by 12 months of age, significant neuronal death after 12 months of age), as well as males developing tau pathology more consistently than females. It is not determined if these phenotype differences are observed for the PS19 colony at The Jackson Laboratory. To ensure genetically stability, we periodically refresh our colony onto the hybrid B6C3F1/J genetic background (Stock No. 100010). This was last performed March to November 2016.
Development
The P301S transgene was designed with the P301S mutant human microtubule-associated protein tau (MAPT*P301S) under the direction of the mouse prion protein promoter (Prnp). This transgene was injected into fertilized B6C3F1 mouse eggs. Transgenic founder animals were bred to B6C3F1/J or B6C3F1/Crl mice to establish founder line 19 (PS19). The resulting PS19 colony was maintained as hemizygotes on the B6C3F1 background before sending to The Jackson Laboratory Repository in 2008.
Expression Data
| Expressed Gene | MAPT, microtubule associated protein tau, human |
|---|---|
| Site of Expression |
Control Suggestions
Selected References
- Yoshiyama Y; Higuchi M; Zhang B; Huang SM; Iwata N; Saido TC; Maeda J; Suhara T; Trojanowski JQ; Lee VM. 2007. Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model. Neuron 53(3):337-51. PubMed: 17270732MGI: J:119741
Tg(Prnp-MAPT*P301S)PS19Vle
Allele Symbol: Tg(Prnp-MAPT*P301S)PS19Vle
| Allele Name | transgene insertion PS19, Virginia M Y Lee |
|---|---|
| Allele Type | Transgenic (Humanized sequence, Inserted expressed sequence) |
| Allele Synonym(s) | P301S tau (line PS19); PS19 Tg |
| Gene Symbol and Name | Tg(Prnp-MAPT*P301S)PS19Vle, transgene insertion PS19, Virginia M Y Lee |
| Gene Synonym(s) | P301S tau (line PS19); PS19 Tg |
| Promoter | Prnp, prion protein, mouse, laboratory |
| Expressed Gene | MAPT, microtubule associated protein tau, human |
| Strain of Origin | (C57BL/6 x C3H)F1 |
| Chromosome | UN |
| Molecular Note | The transgene construct contains the P301S mutant human microtubule-associated protein tau, MAPT, under the direction of the mouse prion protein, Prnp, promoter. The expression of the mutant human MAPT is 5-fold higher than the expression of the endogenous mouse Mapt protein. |
| Mutations Made By | Virginia Lee, University of Pennsylvania |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Neurobiology Research
- Alzheimer's Disease
- Neurodegeneration
Genotype: MAPT related
- Neurobiology Research
- Alzheimer's Disease
- Parkinson's Disease
Genotype: Tg(Prnp-MAPT*P301S)PS19Vle related
- Neurobiology Research
- Alzheimer's Disease
- Tau (Mapt) mutants
- Alzheimer's Disease
Mammalian Phenotype Terms by Genotype
Genotype: Tg(Prnp-MAPT*P301S)PS19Vle/0
involves: C3H * C57BL/6
mortality/aging
- premature death
behavior/neurological phenotype
- abnormal spatial learning
- 6 month old females are able to learn to locate the platform of the Morris water maze during training and latencies to find the visible platform are similar between mutants and wild-type mice, however mutants spend more time in finding the invisible platform, indicating impaired spatial learning abilityorm, indicating impaired spatial learning ability (MGI Ref ID J:174441)
- during the probe trail of the Morris water maze, mutant females show less time and path length in the pool quadrant where the platform had previously been placed and a smaller number of target platform crossings (MGI Ref ID J:174441)
- hunched posture
- limb grasping
- at 3 months of age, mice exhibit limb grasping and limb retraction when lifted by the tail, whereas mice expressing a wild-type MAPT transgene show no neurodegenerative phenotype up to 24 months of age (MGI Ref ID J:119741)
- paralysis
- paresis
- 44% of mutants exhibit paresis or paralysis and presence of a hunchback posture at 11 months of age (MGI Ref ID J:165441)
- weakness
- limb grasping at 3 months of age is followed by limb weakness (MGI Ref ID J:119741)
nervous system phenotype
- abnormal CNS synaptic transmission
- abnormal amygdala morphology
- neuron loss is observed at 12 months of age (MGI Ref ID J:119741)
- abnormal cerebral cortex morphology
- abnormal dentate gyrus morphology
- at 3 months, mice have neurofilament light chain and tau-positive spheroids in the dentate gyrus, as well as in the cortex (MGI Ref ID J:119741)
- abnormal entorhinal cortex morphology
- neuron loss is observed at 12 months of age (MGI Ref ID J:119741)
- abnormal excitatory postsynaptic potential
- at 6 months, the maximum fEPSP is reduced relative to wild-type MAPT transgenic mice (MGI Ref ID J:119741)
- abnormal hippocampal mossy fiber morphology
- at 3 months but not at 6 months, neurofilament light chain-positive mossy fibers are not detected in CA3 of hippocampus at 3 months but not at 6 months, neurofilament light chain-positive mossy fibers are not detected in CA3 of hippocampusat 3 months but not at 6 months, neurofilament light chain-positive mossy fibers are not detected in CA3 of hippocampus (MGI Ref ID J:119741)
- abnormal hippocampus pyramidal cell morphology
- significant reduction in number in the hippocampal CA3 region is found at 12 months of age, but no loss is detected at 6 months (MGI Ref ID J:119741)
- abnormal spinal cord white matter morphology
- at 3 months, mice have neurofilament light chain and tau-positive spheroids in the spinal cord white matter (MGI Ref ID J:119741)
- astrocytosis
- gliosis is striking at 6 months in the white matter where little tau pathology exists (MGI Ref ID J:119741)
- microglial activation precedes astrogliosis in brain regions containing NFTs; this is found in the brain and spinal cord, especially in white matter at 3 months of age with increases seen at 6 months in white and gray matter of hippocampus, amygdala, entorhinal cortex and spinal cordrhinal cortex and spinal cord (MGI Ref ID J:119741)
- younger mice (3-4 months) show no overt gliosis but increased microglial activation is detected in the hippocampus (MGI Ref ID J:119741)
- brain atrophy
- limb grasping at 3 months of age is followed by brain atrophy (MGI Ref ID J:119741)
- decreased hippocampus volume
- ~25% and ~40% reductions in hippocampal volume at 9 and 12 months of age respectively (MGI Ref ID J:119741)
- decreased paired-pulse facilitation
- at 6 months, mice show significantly reduce paired pulse facilitation (PPF) ratio at all stimulus intervals (MGI Ref ID J:119741)
- dilated brain ventricles
- by 8 months of age, ventricular dilatation is seen (MGI Ref ID J:119741)
- hippocampal neuron degeneration
- (MGI Ref ID J:119741)
- hippocampus atrophy
- marked hippocampal atrophy at 9 months of age (MGI Ref ID J:119741)
- loss of hippocampal neurons
- up to 6 months, mice show no neuron loss, but by 8 months of age, neuron loss in the hippocampus is seen, becoming more severe in hippocampus, as well as amygdala, neocortex and entorhinal cortex by 12 months of age (MGI Ref ID J:119741)
- neurodegeneration
- mice show progressive neurodegeneration starting at 1 month of age, as determined by increasing loss of synaptophysin immunoreactivity (MGI Ref ID J:119741)
- neurofibrillary tangles
- at 6 months of age, neurofibrillary tangles (NFT) are evident in neocortex, amygdala, hippocampus, brain stem and spinal cord but none are found in mice expressing wild-type human MAPT up to 24 months of age (MGI Ref ID J:119741)
- mutants develop ThS-positive neurofibrillary tangles (MGI Ref ID J:165441)
- reduced long term potentiation
- LTP in CA1 region of hippocampus is significantly deteriorated, indicating attenuated postsynaptic responsiveness and compromised synaptic plasticity, but at 6 months no overt reduction in neuron number is detected (MGI Ref ID J:119741)
- tau protein deposits
- aggregation of insoluble tau in the cortex and hippocampus (MGI Ref ID J:233816)
- at 3 months of age, mutants and mice expressing wild-type transgenic human tau show weak perikaryal and dendritic tau staining mainly in hippocampus, amygdala, cortex, brain stem, and spinal cord; at 6 months, mutants show stronger tau-positive neuronal staining in the hippocampus, amygdala, and spinal cord but older mice expressing wild-type human tau protein show no increases up to 12 monthstaining in the hippocampus, amygdala, and spinal cord but older mice expressing wild-type human tau protein show no increases up to 12 months (MGI Ref ID J:119741)
- mutants exhibit progression in the distribution of abnormally phosphorylated tau from the entorhinal and neocortex, followed by involvement of the hippocampal formation and subcortical structures, to finally penetration of all layers of the neocortex (MGI Ref ID J:165441)
- with aging, brains of mice have increasing levels of insoluble tau deposits composed mainly of transgenic human tau; decrease in solubility of tau is observed between 3 and 6 months (MGI Ref ID J:119741)
muscle phenotype
- dystrophic muscle
- affected muscles show group atrophies with small angular fibers, indicating chronic denervation of motor neurons (MGI Ref ID J:119741)
- progressive muscle weakness
- mice show motor increasing weakness and neurogenic muscular atrophy after 3 months of age (MGI Ref ID J:119741)
growth/size/body region phenotype
- weight loss
- slight decrease in weight is seen at 11 months of age (MGI Ref ID J:165441)
Genotype: Tg(Prnp-MAPT*P301S)PS19Vle/Tg(Prnp-MAPT*P301S)PS19Vle
involves: C3H * C57BL/6
behavior/neurological phenotype
- abnormal sexual interaction
- homozygous females do not mate, so mice have to be maintained as hemizygotes (MGI Ref ID J:119741)
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Tg(Prnp-MAPT*P301S)PS19Vle/0
B6.Cg-Tg(Prnp-MAPT*P301S)PS19Vle
behavior/neurological phenotype
- abnormal behavior
- in the Barnes circular maze test, males are able to locate the correct target hole where the escape box had been in the probe trial, however they spend less time around the target hole than wild-type mice (MGI Ref ID J:174441)
- in the Y-maze test, the total percentage of alternations is decreased indicating impaired spontaneous alternation (MGI Ref ID J:174441)
- abnormal contextual conditioning behavior
- in the contextual fear conditioning test, mutants show decreased immobility in the fourth time point only (MGI Ref ID J:174441)
- abnormal emotion/affect behavior
- in a portion of the Porsolt forced swim test, mutants show decreased immobility time and increased distance traveled, suggesting that despair-like behavior might be decreased, however, generally over the entire test, no statistical significance is seen for immobilityr immobility (MGI Ref ID J:174441)
- abnormal social investigation
- however, no differences were seen in the social interaction test of a one-chamber novel environment (MGI Ref ID J:174441)
- in Crawley's three-chamber social approach test, males spend a shorter time with stranger mice than with familiar mice compared to wild-type mice which spend more time with stranger mice, indicating some impaired sociability or object recognition memory (MGI Ref ID J:174441)
- decreased anxiety-related response
- in the elevated plus-maze test, entries into and time spent on the open arms is increased and in the open field test, time spent in the center of the field is increased, indicating decreased anxiety-like behavior (MGI Ref ID J:174441)
- decreased thermal nociceptive threshold
- males exhibit decreased thresholds in the hot plate test, indicating increased antinociceptive responses (MGI Ref ID J:174441)
- hyperactivity
- in the Y-maze test, males show increased numbers of entries into each arm, total alternations, and total distance traveled indicating hyperactivity (MGI Ref ID J:174441)
- in the open field test, 14 week old males show an increase in total locomotive distance and an increase in stereotypic locomotion (MGI Ref ID J:174441)
- increased vertical activity
- vertical activity of 14 week old males is increased in the latter half of the open field test (MGI Ref ID J:174441)
integument phenotype
- decreased thermal nociceptive threshold
- males exhibit decreased thresholds in the hot plate test, indicating increased antinociceptive responses (MGI Ref ID J:174441)
nervous system phenotype
- increased prepulse inhibition
- males younger than 6 months of age exhibit lower startle amplitudes than wild-type mice at 110 dB and 120 dB and an increase in percent prepulse inhibition (MGI Ref ID J:174441)
- tau protein deposits
- hyperphosphorylated tau protein accumulation is seen in the lateral globus pallidus, amygdala, auditory cortex, ventral hippocampus, the cingulate cortex, anterior cortical amygdaloid nucleus, and dorsal hippocampus at 4 months of age (MGI Ref ID J:174441)
References
- Yoshiyama Y; Higuchi M; Zhang B; Huang SM; Iwata N; Saido TC; Maeda J; Suhara T; Trojanowski JQ; Lee VM. 2007. Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model. Neuron 53(3):337-51. PubMed: 17270732MGI: J:119741
Additional - Tg(Prnp-MAPT*P301S)PS19Vle related
- Caccamo A; Magri A; Medina DX; Wisely EV; Lopez-Aranda MF; Silva AJ; Oddo S. 2013. mTOR regulates tau phosphorylation and degradation: implications for Alzheimer's disease and other tauopathies. Aging Cell 12(3):370-80. PubMed: 23425014MGI: J:218147
- Carroll JC; Iba M; Bangasser DA; Valentino RJ; James MJ; Brunden KR; Lee VM; Trojanowski JQ. 2011. Chronic Stress Exacerbates Tau Pathology, Neurodegeneration, and Cognitive Performance through a Corticotropin-Releasing Factor Receptor-Dependent Mechanism in a Transgenic Mouse Model of Tauopathy. J Neurosci 31(40):14436-49. PubMed: 21976528MGI: J:177434
- Chakravarthy B; Gaudet C; Menard M; Brown L; Atkinson T; Laferla FM; Ito S; Armato U; Dal Pra I; Whitfield J. 2012. Reduction of the immunostainable length of the hippocampal dentate granule cells' primary cilia in 3xAD-transgenic mice producing human Abeta(1-42) and tau. Biochem Biophys Res Commun 427(1):218-22. PubMed: 22995307MGI: J:190096
- Cohen TJ; Guo JL; Hurtado DE; Kwong LK; Mills IP; Trojanowski JQ; Lee VM. 2011. The acetylation of tau inhibits its function and promotes pathological tau aggregation. Nat Commun 2:252. PubMed: 21427723MGI: J:226145
- Dumont M; Stack C; Elipenahli C; Jainuddin S; Gerges M; Starkova N; Calingasan NY; Yang L; Tampellini D; Starkov AA; Chan RB; Di Paolo G; Pujol A; Beal MF. 2012. Bezafibrate administration improves behavioral deficits and tau pathology in P301S mice. Hum Mol Genet 21(23):5091-105. PubMed: 22922230MGI: J:188924
- Dumont M; Stack C; Elipenahli C; Jainuddin S; Gerges M; Starkova NN; Yang L; Starkov AA; Beal F. 2011. Behavioral deficit, oxidative stress, and mitochondrial dysfunction precede tau pathology in P301S transgenic mice. FASEB J 25(11):4063-72. PubMed: 21825035MGI: J:178410
- Frake RA; Ricketts T; Menzies FM; Rubinsztein DC. 2015. Autophagy and neurodegeneration. J Clin Invest 125(1):65-74. PubMed: 25654552MGI: J:219892
- Holmes BB; Furman JL; Mahan TE; Yamasaki TR; Mirbaha H; Eades WC; Belaygorod L; Cairns NJ; Holtzman DM; Diamond MI. 2014. Proteopathic tau seeding predicts tauopathy in vivo. Proc Natl Acad Sci U S A 111(41):E4376-85. PubMed: 25261551MGI: J:216453
- Hurtado DE; Molina-Porcel L; Carroll JC; Macdonald C; Aboagye AK; Trojanowski JQ; Lee VM. 2012. Selectively Silencing GSK-3 Isoforms Reduces Plaques and Tangles in Mouse Models of Alzheimer's Disease. J Neurosci 32(21):7392-402. PubMed: 22623685MGI: J:184975
- Hurtado DE; Molina-Porcel L; Iba M; Aboagye AK; Paul SM; Trojanowski JQ; Lee VM. 2010. A{beta} accelerates the spatiotemporal progression of tau pathology and augments tau amyloidosis in an Alzheimer mouse model. Am J Pathol 177(4):1977-88. PubMed: 20802182MGI: J:165441
- Iba M; Guo JL; McBride JD; Zhang B; Trojanowski JQ; Lee VM. 2013. Synthetic tau fibrils mediate transmission of neurofibrillary tangles in a transgenic mouse model of Alzheimer's-like tauopathy. J Neurosci 33(3):1024-37. PubMed: 23325240MGI: J:213838
- Ji B; Maeda J; Sawada M; Ono M; Okauchi T; Inaji M; Zhang MR; Suzuki K; Ando K; Staufenbiel M; Trojanowski JQ; Lee VM; Higuchi M; Suhara T. 2008. Imaging of peripheral benzodiazepine receptor expression as biomarkers of detrimental versus beneficial glial responses in mouse models of Alzheimer's and other CNS pathologies. J Neurosci 28(47):12255-67. PubMed: 19020019MGI: J:142367
- Jiang T; Tan L; Zhu XC; Zhou JS; Cao L; Tan MS; Wang HF; Chen Q; Zhang YD; Yu JT. 2015. Silencing of TREM2 exacerbates tau pathology, neurodegenerative changes, and spatial learning deficits in P301S tau transgenic mice. Neurobiol Aging 36(12):3176-86. PubMed: 26364736MGI: J:232244
- Koss DJ; Robinson L; Drever BD; Plucinska K; Stoppelkamp S; Veselcic P; Riedel G; Platt B. 2016. Mutant Tau knock-in mice display frontotemporal dementia relevant behaviour and histopathology. Neurobiol Dis 91:105-23. PubMed: 26949217MGI: J:240857
- Maeda J; Zhang MR; Okauchi T; Ji B; Ono M; Hattori S; Kumata K; Iwata N; Saido TC; Trojanowski JQ; Lee VM; Staufenbiel M; Tomiyama T; Mori H; Fukumura T; Suhara T; Higuchi M. 2011. In Vivo Positron Emission Tomographic Imaging of Glial Responses to Amyloid-{beta} and Tau Pathologies in Mouse Models of Alzheimer's Disease and Related Disorders. J Neurosci 31(12):4720-4730. PubMed: 21430171MGI: J:170310
- Maeda S; Djukic B; Taneja P; Yu GQ; Lo I; Davis A; Craft R; Guo W; Wang X; Kim D; Ponnusamy R; Gill TM; Masliah E; Mucke L. 2016. Expression of A152T human tau causes age-dependent neuronal dysfunction and loss in transgenic mice. EMBO Rep 17(4):530-51. PubMed: 26931567MGI: J:233816
- Mewes A; Franke H; Singer D. 2012. Organotypic brain slice cultures of adult transgenic P301S mice--a model for tauopathy studies. PLoS One 7(9):e45017. PubMed: 22984603MGI: J:192890
- Mikhail F; Calingasan N; Parolari L; Subramanian A; Yang L; Flint Beal M. 2015. Lack of exacerbation of neurodegeneration in a double transgenic mouse model of mutant LRRK2 and tau. Hum Mol Genet 24(12):3545-56. PubMed: 25804954MGI: J:221597
- Min SW; Cho SH; Zhou Y; Schroeder S; Haroutunian V; Seeley WW; Huang EJ; Shen Y; Masliah E; Mukherjee C; Meyers D; Cole PA; Ott M; Gan L. 2010. Acetylation of tau inhibits its degradation and contributes to tauopathy. Neuron 67(6):953-66. PubMed: 20869593MGI: J:167861
- Rousseaux MW; de Haro M; Lasagna-Reeves CA; De Maio A; Park J; Jafar-Nejad P; Al-Ramahi I; Sharma A; See L; Lu N; Vilanova-Velez L; Klisch TJ; Westbrook TF; Troncoso JC; Botas J; Zoghbi HY. 2016. TRIM28 regulates the nuclear accumulation and toxicity of both alpha-synuclein and tau. Elife 5:. PubMed: 27779468MGI: J:238738
- Sanders DW; Kaufman SK; DeVos SL; Sharma AM; Mirbaha H; Li A; Barker SJ; Foley AC; Thorpe JR; Serpell LC; Miller TM; Grinberg LT; Seeley WW; Diamond MI. 2014. Distinct tau prion strains propagate in cells and mice and define different tauopathies. Neuron 82(6):1271-88. PubMed: 24857020MGI: J:221275
- Saul A; Sprenger F; Bayer TA; Wirths O. 2013. Accelerated tau pathology with synaptic and neuronal loss in a novel triple transgenic mouse model of Alzheimer's disease. Neurobiol Aging 34(11):2564-73. PubMed: 23747045MGI: J:211723
- Stack C; Jainuddin S; Elipenahli C; Gerges M; Starkova N; Starkov AA; Jove M; Portero-Otin M; Launay N; Pujol A; Kaidery NA; Thomas B; Tampellini D; Beal MF; Dumont M. 2014. Methylene blue upregulates Nrf2/ARE genes and prevents tau-related neurotoxicity. Hum Mol Genet 23(14):3716-32. PubMed: 24556215MGI: J:210668
- Tagawa K; Homma H; Saito A; Fujita K; Chen X; Imoto S; Oka T; Ito H; Motoki K; Yoshida C; Hatsuta H; Murayama S; Iwatsubo T; Miyano S; Okazawa H. 2015. Comprehensive phosphoproteome analysis unravels the core signaling network that initiates the earliest synapse pathology in preclinical Alzheimer's disease brain. Hum Mol Genet 24(2):540-58. PubMed: 25231903MGI: J:217304
- Takeuchi H; Iba M; Inoue H; Higuchi M; Takao K; Tsukita K; Karatsu Y; Iwamoto Y; Miyakawa T; Suhara T; Trojanowski JQ; Lee VM; Takahashi R. 2011. P301S mutant human tau transgenic mice manifest early symptoms of human tauopathies with dementia and altered sensorimotor gating. PLoS One 6(6):e21050. PubMed: 21698260MGI: J:174441
- Wang H; Wang R; Carrera I; Xu S; Lakshmana MK. 2016. TFEB Overexpression in the P301S Model of Tauopathy Mitigates Increased PHF1 Levels and Lipofuscin Puncta and Rescues Memory Deficits. eNeuro 3(2):. PubMed: 27257626MGI: J:240197
- Wisely EV; Xiang YK; Oddo S. 2014. Genetic suppression of beta2-adrenergic receptors ameliorates tau pathology in a mouse model of tauopathies. Hum Mol Genet 23(15):4024-34. PubMed: 24626633MGI: J:210986
- Xu L; Ryu J; Nguyen JV; Arena J; Rha E; Vranis P; Hitt D; Marsh-Armstrong N; Koliatsos VE. 2015. Evidence for accelerated tauopathy in the retina of transgenic P301S tau mice exposed to repetitive mild traumatic brain injury. Exp Neurol 273:168-76. PubMed: 26311071MGI: J:229560
- Yamada K; Cirrito JR; Stewart FR; Jiang H; Finn MB; Holmes BB; Binder LI; Mandelkow EM; Diamond MI; Lee VM; Holtzman DM. 2011. In vivo microdialysis reveals age-dependent decrease of brain interstitial fluid tau levels in P301S human tau transgenic mice. J Neurosci 31(37):13110-7. PubMed: 21917794MGI: J:191549
- Yata K; Oikawa S; Sasaki R; Shindo A; Yang R; Murata M; Kanamaru K; Tomimoto H. 2011. Astrocytic neuroprotection through induction of cytoprotective molecules; a proteomic analysis of mutant P301S tau-transgenic mouse. Brain Res 1410:12-23. PubMed: 21803337MGI: J:175758
- Yoshiyama Y; Kojima A; Itoh K; Uchiyama T; Arai K. 2012. Anticholinergics boost the pathological process of neurodegeneration with increased inflammation in a tauopathy mouse model. Neurobiol Dis 45(1):329-36. PubMed: 21889983MGI: J:179843
- Zhang B; Carroll J; Trojanowski JQ; Yao Y; Iba M; Potuzak JS; Hogan AM; Xie SX; Ballatore C; Smith AB 3rd; Lee VM; Brunden KR. 2012. The microtubule-stabilizing agent, epothilone D, reduces axonal dysfunction, neurotoxicity, cognitive deficits, and Alzheimer-like pathology in an interventional study with aged tau transgenic mice. J Neurosci 32(11):3601-11. PubMed: 22423084MGI: J:213839
- Zhang Z; Song M; Liu X; Kang SS; Kwon IS; Duong DM; Seyfried NT; Hu WT; Liu Z; Wang JZ; Cheng L; Sun YE; Yu SP; Levey AI; Ye K. 2014. Cleavage of tau by asparagine endopeptidase mediates the neurofibrillary pathology in Alzheimer's disease. Nat Med 20(11):1254-62. PubMed: 25326800MGI: J:227814