Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model

By E. Roberson, K. Scearce-Levie, J. Palop, Fengrong Yan, I. Cheng, Tiffany Wu, H. Gerstein, Gui-qiu Yu, L. Mucke. Science, 2007

1,956 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/d54bc5fb504e3b69a9c8ac3f7e0c77acde28fd47

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Citations in the corpus

Pathogenic Protein Seeding in Alzheimer’s Disease and Other Neurodegenerative Disorders (2011, background): “Moreover, at least some of the Ab toxicity appears to be tau dependent.(19,20) Cross-sectional analyses of postmortem human brains reveal a characteristic progression of Ab plaques and a highly stereotypical appearance of neurofibrillary tangles (Fig 1).”
Post-translational modifications of tau protein: implications for Alzheimer's disease. (2011, unknown): “However, tau protein regardless of its post-translational modifications, can also be toxic per se (Amadoro et al., 2006), and the suppression of tau protein blocks Ab-induced apoptosis (Rapoport et al., 2002) and reduces memory deficit (Roberson et al., 2007; Santacruz et al., 2005).”
Neurotoxicity of amyloid β-protein: synaptic and network dysfunction. (2012, background): “Tau reduction has also been shown to make mice with or without hAPP/Ab overexpression more resistant to chemically induced seizures (Roberson et al. 2007; Ittner et al. 2010), suggesting a previously unrecognized role of tau in the regulation of neuronal activity.”
Epilepsy and Cognitive Impairments in Alzheimer Disease (2009, background): “Our experimental data suggest that reducing tau levels is highly effective in preventing A -induced network dysfunction and cognitive deficits in vivo (Figure 3).(4,5) However, much more research is needed to further assess the efficacy and safety of this novel therapeutic strategy.”
Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “Moreover, when transgenic mice that overexpress APP are crossed with mice lacking tau, no detioration in spatial memory function is seen even though Aβ deposition is exuberant (Roberson et al. 2007).”
Aβ Oligomers Cause Localized Ca2+ Elevation, Missorting of Endogenous Tau into Dendrites, Tau Phosphorylation, and Destruction of Microtubules and Spines (2010, background): “…conversely Tau is considered necessary for the progression of neurodegeneration, as seen in cell and animal models (Rapoport et al., 2002; King et al., 2006; Roberson et al., 2007), and indeed the Tau pathology correlates well with clinical symptoms (Braak and Braak, 1991; Clavaguera et al., 2009).”
Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease (2018, background): “Indeed, it has already been reported that the suppression or deletion of tau has a profound protective effect against brain damage and neurological deficits (Rapoport et al., 2002; SantaCruz et al., 2005; Roberson et al., 2007; Miao et al., 2010; Shipton et al., 2011; Bi et al., 2017).”