Enhanced Neurofibrillary Degeneration in Transgenic Mice Expressing Mutant Tau and APP

By Jada Lewis, Dennis W. Dickson, Wen‐lang Lin, L. Chisholm, A. Corral, G. Jones, S. Yen, N. Sahara, L. Skipper, D. Yager and 4 more. Science, 2001

1,666 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/76d22bedfcfbe9f1ad91288e4f27fc25601eb920

How researchers see this paper

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

In Cellular and Molecular Neuroscience

1. D. Selkoe
2. G. Shankar
3. E. Mandelkow
4. Nina E. Shepardson
5. L. Ittner
6. J. Götz
7. V. Lee
8. D. Walsh

In Molecular Biology

1. D. Selkoe
2. John Q. Trojanowski
3. E. Mandelkow
4. L. Ittner
5. K. Del Tredici
6. J. Götz
7. F. LaFerla
8. H. Braak

In Physiology

1. D. Selkoe
2. E. Mandelkow
3. John Q. Trojanowski
4. L. Ittner
5. J. Götz
6. K. Del Tredici
7. John Hardy
8. G. Shankar

Citations in the corpus

• Amyloid deposition precedes tangle formation in a triple transgenic model of Alzheimer's disease. (2003, background): “The same appears to be true in other mouse models [1,4].”
• Alzheimer’s and Parkinson’s diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein (2015, neutral): “The crossing of lines expressing mutant tau with lines expressingmutantAPP resulted in enhanced tau pathology (68).”
• Alzheimer’s Disease and the β-Amyloid Peptide (2010, neutral): “Transgenic mice have been used to demonstrate convincingly that Aβ increases the rate of neurofibrillary tangle pathology in mice which also express mutant tau protein [124,125], placing Aβ pathology firmly upstream of tangle pathology in the hierarchy of disease progression.”
• Aβ Oligomers – a decade of discovery (2007, background): “…Ab into the brains of tau transgenic mice or co-expression of mutant APP with mutant tau accelerates tau hyperphosphorylation and leads to tangle formation reminiscent of the other hallmark lesion that characterizes AD (Gotz et al. 2001; Lewis et al. 2001; Oddo et al. 2003; Santacruz et al. 2005).”
• Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, neutral): “neurodegeneration is enhanced in mice with both pathologies, whereas amyloid pathology is generally unaffected(Bolmont et al., 2007; Götz et al., 2001; Hurtado et al., 2010; Lewis et al., 2001; Pooler et al., 2015).”
• APP mouse models for Alzheimer's disease preclinical studies (2017, neutral): “In efforts to replicate NFT pathology, crossbreeding of mutant Tau-Tg mice with APP-Tg mice enhanced tau pathology in the limbic system and olfactory cortex without affecting A b pathology (Tg2576 and JNPL3: Lewis et al , 2001; APP23 and JNPL3: Bolmont et al , 2007).”
• The amyloid hypothesis for Alzheimer’s disease: a critical reappraisal (2009, background): “…time that substantial Ab induced degeneration has been seen is in the 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…”