Results 21 to 30 of about 78,455 (315)

The Future of Seed Amplification Assays and Clinical Trials

Frontiers in Aging Neuroscience, 2022
Prion-like seeded misfolding of host proteins is the leading hypothesised cause of neurodegenerative diseases. The exploitation of the mechanism in the protein misfolding cyclic amplification (PMCA) and real-time quaking-induced conversion (RT-QuIC ...
Thomas Coysh, Thomas Coysh, Simon Mead, Simon Mead   +3 more
doaj   +1 more source

Simultaneous expression of MMB-FOXM1 complex components enables efficient bypass of senescence

Scientific Reports, 2021
Cellular senescence is a stable cell cycle arrest that normal cells undergo after a finite number of divisions, in response to a variety of intrinsic and extrinsic stimuli. Although senescence is largely established and maintained by the p53/p21WAF1/CIP1
Ruchi Kumari, Holger Hummerich, Xu Shen, Martin Fischer, Larisa Litovchick, Sibylle Mittnacht, James A. DeCaprio, Parmjit S. Jat   +7 more
doaj   +1 more source

NT1-Tau Is Increased in CSF and Plasma of CJD Patients, and Correlates with Disease Progression

Cells, 2021
This study investigates the diagnostic and prognostic potential of different forms of tau in biofluids from patients with Creutzfeldt-Jakob disease (CJD).
David Mengel, Tze How Mok, Akin Nihat, Wen Liu, Robert A. Rissman, Douglas Galasko, Henrik Zetterberg, Simon Mead, John Collinge, Dominic M. Walsh   +9 more
doaj   +1 more source

Computational Studies of the Structural Stability of Rabbit Prion Protein Compared to Human and Mouse Prion Proteins [PDF]

, 2011
Prion diseases are invariably fatal and highly infectious neurodegenerative diseases affecting humans and animals. The neurodegenerative diseases such as Creutzfeldt-Jakob disease, variant Creutzfeldt-Jakob diseases, Gerstmann-Str$\ddot{a}$ussler ...
Zhang, Jiapu
core   +2 more sources

Prion Diseases [PDF]

Continuum, 2015
This article presents an update on the clinical aspects of human prion disease, including the wide spectrum of their presentations.Prion diseases, a group of disorders caused by abnormally shaped proteins called prions, occur in sporadic (Jakob-Creutzfeldt disease), genetic (genetic Jakob-Creutzfeldt disease, Gerstmann-Sträussler-Scheinker syndrome ...
openaire   +7 more sources

Structural insights into how augmin augments the mitotic spindle

Nature Communications, 2023
Cell division critically requires amplification of microtubules (MTs) in the bipolar mitotic spindle. This relies on the filamentous augmin complex that enables MT branching. Studies by Gabel et al., Zupa et al. and Travis et al.
Szymon W. Manka
doaj   +1 more source

ALK1 controls hepatic vessel formation, angiodiversity, and angiocrine functions in hereditary hemorrhagic telangiectasia of the liver

Hepatology, EarlyView., 2022
Hepatic endothelial Alk1 signaling protects from development of vascular malformations while maintaining organ‐specific endothelial differentiation and angiocrine portmanteau of the names Wingless and Int‐1 signaling. Abstract Background and Aims In hereditary hemorrhagic telangiectasia (HHT), severe liver vascular malformations are associated with ...
Christian David Schmid, Victor Olsavszky, Manuel Reinhart, Vanessa Weyer, Felix A. Trogisch, Carsten Sticht, Manuel Winkler, Sina W. Kürschner, Johannes Hoffmann, Roxana Ola, Theresa Staniczek, Joerg Heineke, Beate K. Straub, Jens Mittler, Kai Schledzewski, Peter ten Dijke, Karsten Richter, Steven Dooley, Cyrill Géraud, Sergij Goerdt, Philipp‐Sebastian Koch   +20 more
wiley   +1 more source

A blood miRNA signature associates with sporadic Creutzfeldt-Jakob disease diagnosis

Nature Communications, 2020
Sporadic Creutzfeldt-Jakob disease (sCJD) is a rapidly progressive dementia. No clinical blood tests are available for diagnosis. The authors identified three miRNAs in whole-blood that are downregulated in sCJD patients, and discriminate sCJD from ...
Penny J. Norsworthy, Andrew G. B. Thompson, Tze H. Mok, Fernando Guntoro, Luke C. Dabin, Akin Nihat, Ross W. Paterson, Jonathan M. Schott, John Collinge, Simon Mead, Emmanuelle A. Viré   +10 more
doaj   +1 more source

Heat shock factor 1 regulates lifespan as distinct from disease onset in prion disease [PDF]

, 2008
Prion diseases are fatal, transmissible, neurodegenerative diseases caused by the misfolding of the prion protein (PrP). At present, the molecular pathways underlying prion-mediated neurotoxicity are largely unknown.
Aguzzi, Adriano, Borkowski, Andrew W., Heppner, Frank L., Hutter, Gregor, Jackson, Walter S., King, Oliver D., Lindquist, Susan, Raymond, Gregory J., Steele, Andrew D.   +8 more
core   +3 more sources

A cationic tetrapyrrole inhibits toxic activities of the cellular prion protein [PDF]

, 2016
Prion diseases are rare neurodegenerative conditions associated with the conformational conversion of the cellular prion protein (PrPC) into PrPSc, a self-replicating isoform (prion) that accumulates in the central nervous system of affected individuals.
Biasini, Emiliano, Borsello, Tiziana, Castilla, Joaqu\uedn, Cerovic, Milica, Cimini, Sara, Elezgarai, Saioa R., Gobbi, Marco, Massignan, Tania, Moreno, Jorge, Negro, Alessandro, Nonno, Romolo, Restelli, Elena, Riccardi, Geraldina, Sangiovanni, Valeria, Stincardini, Claudia, Stravalaci, Matteo, Vanni, Ilaria   +16 more
core   +2 more sources