It's the beginning of the end for James Corden's Late Late Show and the last two weeks are set to be jam-packed. With appearances by: 🎤 Blackpink 🎭 Ben Affleck 🎭 Kate Hudson 📺 The Kardashian Family
after eight years at the helm.since 2015 but revealed at the time he had signed a one-year extension.Now it’s been revealed just who will be appearing across the final 12 episodes.
Allison Janney – who has appeared as a guest on the show more than anyone else- will maintain her record when she makes her 15th appearance.
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James Corden described as most 'obnoxious presenter' by directorHe's been described as 'difficult' to work with
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Controversial Channel 4 show renewed for record-breaking 28th series - and return is just weeks awayCHANNEL 4’s The Last Leg has been renewed for a record-breaking 28th series. Hosts Adam Hills, Josh Widdicombe and Alex Brooker will be back on our screens in just a matter of weeks. The quad…
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Early Adulthood Hypertension, Blood Pressure Change, and Late-Life NeuroimagesThis cohort study assesses the association of early adulthood hypertension and blood pressure change with late-life neuroimaging biomarkers and examines potential sex differences among adults aged 50 years and older.
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Common mouse models of tauopathy reflect early but not late human disease - Molecular NeurodegenerationBackground Mouse models that overexpress human mutant Tau (P301S and P301L) are commonly used in preclinical studies of Alzheimer’s Disease (AD) and while several drugs showed therapeutic effects in these mice, they were ineffective in humans. This leads to the question to which extent the murine models reflect human Tau pathology on the molecular level. Methods We isolated insoluble, aggregated Tau species from two common AD mouse models during different stages of disease and characterized the modification landscape of the aggregated Tau using targeted and untargeted mass spectrometry-based proteomics. The results were compared to human AD and to human patients that suffered from early onset dementia and that carry the P301L Tau mutation. Results Both mouse models accumulate insoluble Tau species during disease. The Tau aggregation is driven by progressive phosphorylation within the proline rich domain and the C-terminus of the protein. This is reflective of early disease stages of human AD and of the pathology of dementia patients carrying the P301L Tau mutation. However, Tau ubiquitination and acetylation, which are important to late-stage human AD are not represented in the mouse models. Conclusion AD mouse models that overexpress human Tau using risk mutations are a suitable tool for testing drug candidates that aim to intervene in the early formation of insoluble Tau species promoted by increased phosphorylation of Tau.
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