Neurofibrillary tangles, amyotrophy and progressive motor disturbance in mice expressing mutant (P301L) tau protein

By Jada Lewis, E. McGowan, Julia M. Rockwood, H. Melrose, P. Nacharaju, M. Slegtenhorst, K. Gwinn‐Hardy, M. Murphy, M. Baker, Xin Yu and 8 more. Nature Genetics, 2000

1,320 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/416eb2c750d5c2b7773510d0cea1b347ec4748dc

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. M. Goedert
2. Fiona M Menzies
3. John C. Morris
4. A. Goate
5. John Hardy
6. D. Holtzman
7. Dennis W. Dickson
8. Li-Huei Tsai

In Neurology

1. D. Rubinsztein
2. T. Dawson
3. D. Holtzman
4. Fiona M Menzies
5. John C. Morris
6. John Hardy
7. A. Goate
8. Dennis W. Dickson

In Physiology

1. D. Holtzman
2. M. Goedert
3. A. Goate
4. John C. Morris
5. John Hardy
6. Dennis W. Dickson
7. Thomas Wisniewski
8. Eleanor Drummond

Citations in the corpus

• The amyloid hypothesis for Alzheimer’s disease: a critical reappraisal (2009, background): “…context of additional microtubule associated protein tau (MAPT) mutations (Lewis et al. 2001; Oddo et al. 2003), and in these cases, the MAPT mutations themselves lead to cell death (Lewis et al. 2000) and so this is an experiment where neurons are very severely compromised before toxicity is seen.”
• Rapamycin alleviates toxicity of different aggregate-prone proteins. (2006, background): “Further tests in mouse models of the disorders associated with these aggregate-prone proteins (34,36,37) will be necessary to confirm the beneficial effects of rapamycin or its analogues.”
• Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms (2003, methodology): “Mice expressing mutant tau (Lewis et al. 2000) have provided the most complete mouse models of neurofibrillary tau pathology available thus far.”
• Aberrant Cdk5 activation by p25 triggers pathological events leading to neurodegeneration and neurofibrillary tangles. (2003, background): “2002; Lewis et al., 2000, 2001).”
• Mechanisms of tau-induced neurodegeneration (2009, neutral): “Consistent with this hypothesis, both intracerebral infusion of Ab in FTDP-17 tau mutation P301L-expressing transgenic mice, as well as crossing these animals with APPTg2576 mice (APP Swedish plus London mutations), were found to exacerbate neurofibrillary pathology [54, 104] and, in the triple tran”
• Abundant Tau Filaments and Nonapoptotic Neurodegeneration in Transgenic Mice Expressing Human P301S Tau Protein (2002, background): “Abundant tau filaments have also been described in sections of brainstems and spinal cords from mice transgenic for human P301L tau (Lewis et al., 2000) but not in other mouse lines transgenic for human tau mutants (Götz et al., 2001a,b; Lim et al., 2001; Tanemura et al., 2001, 2002).”