CoChat
Sign Up
Cited by 269

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Characterization of Pathology in Transgenic Mice Over-Expressing Human Genomic and cDNA Tau Transgenes

Duff, K., Knight, H., Refolo, L.M., Sanders, S., Yu, X., Picciano, M., Malester, B., Hutton, M., Adamson, J., Goedert, M., Burki, K., Davies, P.·2000·Neurobiology of Disease
DOI 10.1006/nbdi.1999.0279
Open this paper in CoChat — free account

Abstract

To examine the normal cellular function of tau and its role in pathogenesis, we have created transgenic mice that overexpress a tau transgene derived from a human PAC that contains the coding sequence, intronic regions, and regulatory regions of the human gene. All six isoforms of human tau are represented in the transgenic mouse brain at the mRNA and protein level and the human tau is distributed in neurites and at synapses, but is absent from cell bodies. A comparison between the genomic tau mice and mice that overexpress a tau cDNA transgene shows that overall, the distribution of tau is similar in the two lines, but human tau is located in the somatodendritic compartment of many neurons in the cDNA mice. Tau-immunoreactive axonal swellings were found in the spinal cords of the cDNA mice, which correlated with a hind-limb abnormality, whereas neuropathology was essentially normal in the genomic mice up to 8 months of age.

Overview

Integrity signals

Registry

Crossref · 10.1006/nbdi.1999.0279

Cites

3 of 3 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Humanized tau models such as hTau feature age-dependent tau pathology, neuronal loss and memory deficits.

    “humanized tau models such as the hTau model comprising a P1-derived artificial chromosome (PAC) copy of the human MAPT gene locus in a murine Mapt KO background (Duff, Knight et al. 2000, Tucker, Meyer et al. 2001, Andorfer, Kress et al. 2003) also feature age-dependent tau pathology, neuronal loss and memory deficits (Andorfer, Kress et al. 2003, Andorfer, Acker et al. 2005, Polydoro, Acker et al”

    From SORLA up-regulation suppresses pathological effects in aged tauopathy mouse brain (2026) · cites this paper as Duff, Knight et al. 2000

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 30

  1. Andreadis, 1992, Structure and novel exons of the human tau gene, Biochemistry, 31, 10626, 10.1021/bi00158a027 · DOI
  2. Aranda-Abreu, 1999, Embryonic lethal abnormal vision-like RNA-binding proteins regulate neurite outgrowth and tau expression in PC12 cells, J. Neurosci., 19, 6907, 10.1523/JNEUROSCI.19-16-06907.1999 · DOI · Paper page
  3. Behar, 1995, Cis-acting signals and trans-acting proteins are involved in tau mRNA targeting into neurites of differentiating neuronal cells, Int. J. Dev. Neurosci., 13, 113, 10.1016/0736-5748(95)00001-W · DOI · Paper page
  4. Braak, 1994, A sequence of cytoskeleton changes related to the formation of neurofibrillary tangles and neuropil threads, Acta Neuropathol. (Berl), 87, 554, 10.1007/BF00293315 · DOI
  5. Brion, 1999, Transgenic expression of the shortest human tau affects its compartmentalization and its phosphorylation as in the pretangle stage of Alzheimer's disease, Am. J. Pathol., 154, 255, 10.1016/S0002-9440(10)65272-8 · DOI
  6. Dayanandan, 1999, Mutations in tau reduce its microtubule binding properties in intact cells and affect its phosphorylation, FEBS Lett., 446, 228, 10.1016/S0014-5793(99)00222-7 · DOI
  7. D'Souza, 1999, Missense and silent tau gene mutations cause frontotemporal dementia with parkinsonism-chromosome 17 type, by affecting multiple alternative RNA splicing regulatory elements, Proc. Natl. Acad. Sci. USA, 96, 5598, 10.1073/pnas.96.10.5598 · DOI
  8. Goedert, 1989, Multiple isoforms of human microtubule-associated protein tau: Sequences and localization in neurofibrillary tangles of Alzheimer's disease, Neuron, 3, 519, 10.1016/0896-6273(89)90210-9 · DOI · Paper page
  9. Goedert, 1999, Tau gene mutation in familial progressive subcortical gliosis, Nat. Med., 5, 454, 10.1038/7454 · DOI
  10. Gotz, 1995, Somatodendritic localization and hyperphosphorylation of tau protein in transgenic mice expressing the longest human brain tau isoform, EMBO J., 14, 1304, 10.1002/j.1460-2075.1995.tb07116.x · DOI
  11. Grover, 1999, 5′ splice site mutations in tau associated with the inherited dementia FTDP-17 affect a stem-loop structure that regulates alternative splicing of exon 10, J. Biol. Chem., 274, 15134, 10.1074/jbc.274.21.15134 · DOI
  12. Hardy, 1998, Genetic dissection of Alzheimer's disease and related dementias: Amyloid and its relationship to tau, Nat. Neurosci., 1, 355, 10.1038/1565 · DOI
  13. Hasegawa, 1998, Tau proteins with FTDP-17 mutations have a reduced ability to promote microtubule assembly, FEBS Lett., 437, 207, 10.1016/S0014-5793(98)01217-4 · DOI
  14. Hong, 1998, Mutation-specific functional impairments in distinct tau isoforms of hereditary FTDP-17, Science, 282, 1914, 10.1126/science.282.5395.1914 · DOI
  15. Ikonomovic, 1997, The loss of GluR2(3) immunoreactivity precedes neurofibrillary tangles formation in the entorhinal cortex and hippocampus of Alzheimer's brains, J. Neuropathol. Exp. Neurol., 56, 1018, 10.1097/00005072-199709000-00007 · DOI
  16. Iqbal, 1996, Molecular mechanism of Alzheimer's neurofibrillary degeneration and therapeutic intervention, Ann. N. Y. Acad. Sci., 777, 132, 10.1111/j.1749-6632.1996.tb34411.x · DOI
  17. Jicha, 1997, Alz-50 and MC-1, a new monoclonal antibody raised to paired helical filaments, recognize conformational epitopes on recombinant tau, J. Neurosci. Res., 48, 128, 10.1002/(SICI)1097-4547(19970415)48:2<128::AID-JNR5>3.0.CO;2-E · DOI
  18. Jicha, 1997, Conformation and phosphorylation dependent antibody recognizing the paired helical filaments of Alzheimer's Disease, J. Neurochem., 69, 2087, 10.1046/j.1471-4159.1997.69052087.x · DOI
  19. Jicha, 1999, Sequence requirements for formation of conformational variants of tau similar to those found in Alzheimer's disease, J. Neurosci. Res., 55, 713, 10.1002/(SICI)1097-4547(19990315)55:6<713::AID-JNR6>3.0.CO;2-G · DOI
  20. Kampers, 1999, Assembly of paired helical filaments from mouse tau: Implications for the neurofibrillary pathology in transgenic mouse models for Alzheimer's disease, FEBS Lett., 451, 39, 10.1016/S0014-5793(99)00522-0 · DOI
  21. Kosik, 1989, Tau in situ hybridization in normal and Alzheimer brain: localization in the somatodendritic compartment, Ann. Neurol., 26, 352, 10.1002/ana.410260308 · DOI
  22. Lynch, 1994, Clinical characteristics of a family with chromosome 17-linked disinhibition-dementia-parkinsonism-amyotrophy complex, Neurology, 44, 1878, 10.1212/WNL.44.10.1878 · DOI
  23. Poorkaj, 1998, Tau is a candidate gene for chromosome 17 frontotemporal dementia, Ann. Neurol., 43, 815, 10.1002/ana.410430617 · DOI · Paper page
  24. Reed, 1998, The neuropathology of a chromosome 17-linked autosomal dominant parkinsonism and dementia (“pallido-ponto-nigral degeneration”), J. Neuropathol. Exp. Neurol., 57, 588, 10.1097/00005072-199806000-00006 · DOI
  25. Reed, 1997, Autosomal dominant dementia with widespread neurofibrillary tangles, Ann. Neurol., 42, 564, 10.1002/ana.410420406 · DOI
  26. Spillantini, 1996, Comparison of the neurofibrillary pathology in Alzheimer's disease and familial presenile dementia with tangles, Acta Neuropathol. (Berl), 92, 42, 10.1007/s004010050487 · DOI · Paper page
  27. Spillantini, 1997, Familial multiple system tauopathy with presenile dementia: A disease with abundant neuronal and glial tau filaments, Proc. Natl. Acad. Sci. USA, 94, 4113, 10.1073/pnas.94.8.4113 · DOI
  28. Spillantini, 1998, Tau protein pathology in neurodegenerative diseases, Trends Neurosci., 21, 428, 10.1016/S0166-2236(98)01337-X · DOI · Paper page
  29. Spillantini, 1998, Mutation in the tau gene in familial multiple system tauopathy with presenile dementia, Proc. Natl. Acad. Sci. USA, 95, 7737, 10.1073/pnas.95.13.7737 · DOI · Paper page
  30. Zhou, 1998, Frontotemporal dementia: Neuropil spheroids and presynaptic terminal degeneration, Ann. Neurol., 44, 99, 10.1002/ana.410440116 · DOI

Cited by

Sorted by citations

Metadata

Authors
Duff, K., Knight, H., Refolo, L. M., Sanders, S., Yu, X., Picciano, M., Malester, B., Hutton, M., Adamson, J., Goedert, M., Burki, K., & Davies, P.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2000-04
Volume
7
Issue
2
Pages
87-98
ISSN
0969-9961
DOI
10.1006/nbdi.1999.0279
Cited by
269
References
3
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review