Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function

By K. Santacruz, Jada Lewis, T. Spires, Jennifer B. Paulson, L. Kotilinek, M. Ingelsson, A. Guimaraes, M. DeTure, M. Ramsden, E. McGowan and 9 more. Science, 2005

1,772 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/213e98528b0a0d2c141035b1b70266409044bd37

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. L. Mucke
4. Bradley T. Hyman
5. L. Ittner
6. J. Götz
7. Dennis W. Dickson
8. V. Lee

In Neurology

1. D. Selkoe
2. Dennis W. Dickson
3. D. Holtzman
4. E. Mandelkow
5. V. Lee
6. Berislav Zlokovic
7. A. Sagare
8. J. Götz

In Physiology

1. D. Selkoe
2. D. Holtzman
3. Berislav Zlokovic
4. L. Mucke
5. E. Mandelkow
6. L. Ittner
7. J. Götz
8. Dennis W. Dickson

Citations in the corpus

• The Many Faces of Tau (2011, background): “Tau can bind to the outside and, possibly, also the inside of microtubules, with its N- and C-terminal regions projecting outward (Kar et al., 2003; Santarella et al., 2004).”
• Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020, background): “For instance, reduced spine density and impaired LTP is observed in tau P301L transgenic mice rTg4510 [278].”
• Alzheimer's disease: strategies for disease modification (2010, background): “Similarly, tau transgenic models, such as Tg4510 (Ref”
• Trans-Synaptic Spread of Tau Pathology In Vivo (2012, methodology): “Primers specific to the human transgene (59-CCCAATCACTGCCTATACCC-39 and 59-CCACGAGAATGCGAAGGA-39 as published [11]), or b-actin (59-GCTCTTTTCCAGCCTTCCTT-39 and 59-AGTACTTGCGCTCAGGAGGA-39) were employed in triplicate in 20 ml PCR reactions using 250 nM each primer pair, 8 ml of diluted cDNA and 10 ml”
• Alzheimer’s disease: experimental models and reality (2017, background): “In contrast, NFTs readily form in transgenic mice that express human tau containing mutations associated with FTLD; the most commonly used models being those that express 4R tau with P301L or P301S mutations [49, 91, 92, 135, 177].”
• The blood-brain barrier in health and chronic neurodegenerative disorders. (2008, neutral): “…(Iadecola, 2004; Zlokovic, 2005), accumulation of neurotoxic Ab on blood vessels and in the brain parenchyma (Rovelet-Lecrux et al., 2006; Hardy, 2006; Deane and Zlokovic, 2007), and intraneuronal lesions, or neurofibrillar tangles (Lee et al., 1991; Santacruz et al., 2005; Tanzi, 2005).”
• Tau in Alzheimer Disease and Related Tauopathies (2010, background): “Employing an inducible transgenic mouse model that expressed human four-repeat tau with the P301L mutation, Santacruz and colleagues [57] found that the cognitive deficiencies correlate with the appearance of soluble hyperphosphorylated tau.”
• TDP‐43 immunoreactivity in hippocampal sclerosis and Alzheimer's disease (2007, methodology): “In such cases, there are usually numerous extracellular NFTs.”
• Post-translational modifications of tau protein: implications for Alzheimer's disease. (2011, neutral): “, 2002) and reduces memory deficit (Roberson et al., 2007; Santacruz et al., 2005).”