Formation of Neurofibrillary Tangles in P301L Tau Transgenic Mice Induced by Aβ42 Fibrils

By J. Götz, Feng Chen, J. Dorpe, R. Nitsch. Science, 2001

1,583 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/7881dfb7600de48eb3b0fa1b36b72c8de4ebc1f7

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. D. Holtzman
3. G. Shankar
4. J. Long
5. L. Ittner
6. J. Götz
7. D. Walsh
8. K. Del Tredici

In Molecular Biology

1. D. Holtzman
2. D. Selkoe
3. J. Long
4. L. Ittner
5. David B. Teplow
6. K. Del Tredici
7. J. Götz
8. G. Bitan

In Physiology

1. D. Selkoe
2. D. Holtzman
3. J. Long
4. K. Del Tredici
5. G. Shankar
6. David B. Teplow
7. G. Bitan
8. L. Ittner

Citations in the corpus

• Paradigm shifts in Alzheimer's disease and other neurodegenerative disorders: The emerging role of oligomeric assemblies (2002, positive): “Formation of NFT also has been induced by direct injection of A (cid:1) (1–42) into the brains of transgenic mice expressing human tau (Gotz et al., 2001), although tangle formation in neurons does not necessarily require their proximity to amyloid deposits (Lewis et al., 2001).”
• Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms (2003, background): “Two independent groups ( Gotz et al. 2001; Lewis et al. 2001) have demonstrated that elevated b-amyloid can influence the severity of pathology in mutant tau mice, suggesting a causal relationship between the two pathologies.”
• Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006, background): “Transgenic mice expressing human tau with the P301L frontotemporal dementia mutation develop neurofibrillary tangles when coexpressing an FAD mutant APP transgene (Lewis et al., 2001; Oddo et al., 2003) or after injection with A 42 (Gotz et al., 2001), indicating that A 42 promotes tangle formation.”
• 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’s Disease and the β-Amyloid Peptide (2010, positive): “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.”