210 results on '"Terwel, Dick"'
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2. Aggregated Tau activates NLRP3–ASC inflammasome exacerbating exogenously seeded and non-exogenously seeded Tau pathology in vivo
3. Preclinical models of Alzheimer’s disease for identification and preclinical validation of therapeutic targets: from fine-tuning strategies for validated targets to new venues for therapy
4. List of Contributors
5. CXCR3 promotes plaque formation and behavioral deficits in an Alzheimer's disease model
6. Templated misfolding of Tau by prion-like seeding along neuronal connections impairs neuronal network function and associated behavioral outcomes in Tau transgenic mice
7. Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine
8. The NLRP3 inflammasome modulates tau pathology and neurodegeneration in a tauopathy model
9. Induced LC degeneration in APP/PS1 transgenic mice accelerates early cerebral amyloidosis and cognitive deficits
10. Effects of sub-chronic donepezil on brain Abeta and cognition in a mouse model of Alzheimer’s disease
11. Extracellular phosphorylation of the amyloid β‐peptide promotes formation of toxic aggregates during the pathogenesis of Alzheimer's disease
12. Neuroinflammatory processes in Alzheimer’s disease
13. Axonal transport, tau protein, and neurodegeneration in Alzheimer’s disease
14. Neuroinflammatory and behavioural changes in the Atp7B mutant mouse model of Wilsonʼs disease
15. Restraint stress increases neuroinflammation independently of amyloid β levels in amyloid precursor protein/PS1 transgenic mice
16. PPARγ and RXRγ ligands act synergistically as potent antineoplastic agents in vitro and in vivo glioma models
17. Locus coeruleus degeneration exacerbates olfactory deficits in APP/PS1 transgenic mice
18. Apolipoprotein E Protects against Neuropathology Induced by a High-Fat Diet and Maintains the Integrity of the Blood-Brain Barrier during Aging
19. Identification and isolation of a hyperphosphorylated, conformationally changed intermediate of human protein tau expressed in yeast
20. Aggregated Tau activates NLRP3-ASC inflammasome exacerbating exogenously seeded and non-exogenously seeded Tau pathology in vivo.
21. Long-Term Treatment with Liraglutide, a Glucagon-Like Peptide-1 (GLP-1) Receptor Agonist, Has No Effect on β-Amyloid Plaque Load in Two Transgenic APP/PS1 Mouse Models of Alzheimer’s Disease
22. The GLP-1 receptor agonist liraglutide reduces pathology-specific tau phosphorylation and improves motor function in a transgenic hTauP301L mouse model of tauopathy
23. Templated misfolding of Tau by prion-like seeding along neuronal connections impairs neuronal network function and associated behavioral outcomes in Tau transgenic mice.
24. CXCR3 promotes plaque formation and behavioral deficits in an Alzheimer’s disease model
25. Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism
26. Amyloid activates GSK-3beta to aggravate neuronal tauopathy in bigenic mice.
27. Selective Loss of Noradrenaline Exacerbates Early Cognitive Dysfunction and Synaptic Deficits in APP/PS1 Mice
28. Nitration of Tyrosine 10 Critically Enhances Amyloid β Aggregation and Plaque Formation
29. P2-239: Site-Specific Effect of Amyloid B-Peptide (Aβ) Phosphorylation on Its Conformation and Aggregation
30. Restraint stress increases neuroinflammation independently of amyloid β levels in amyloid precursor protein/PS1 transgenic mice
31. Serine-409 phosphorylation and oxidative damage define aggregation of human protein tau in yeast
32. O4-02-06: Norepinephrine modulates salutary microglial functions in transgenic models of Alzheimer's disease
33. O1-05-07: iNOS gene deficiency modifies amyloid β deposition, cognitive performance and hippocampal long-term potentiation in an APP transgenic mouse model
34. P4‐235: Norepinephrine deficiency aggravates learning and memory impairment independent of amyloid‐beta levels in APP PS1 mice
35. PPARγ and RXRγ ligands act synergistically as potent antineoplastic agentsin vitroandin vivoglioma models
36. P1-128: Humanized yeast cells recapitulate basic mechanisms of the protein Tau phosphorylation-conformation-aggregation cascade
37. O2‐02–05: Amyloid causes tauopathy by activating GSK3
38. Amyloid Activates GSK-3β to Aggravate Neuronal Tauopathy in Bigenic Mice
39. Neurodegeneration and Neuroinflammation in cdk5/p25-Inducible Mice
40. Tau‐4R suppresses proliferation and promotes neuronal differentiation in the hippocampus of tau knockin/ knockout mice
41. Models of beta-amyloid induced Tau-pathology: the long and "folded" road to understand the mechanism.
42. Microtubule Binding and Clustering of Human Tau-4R and Tau-P301L Proteins Isolated from Yeast Deficient in Orthologues of Glycogen Synthase Kinase-3β or cdk5
43. P2-037: Modelling of differential phosphorylation, conformation and aggregation of protein tau in yeast is extended to its binding to microtubuli in vitro
44. P2-033: Molecular determinants of the phosphorylation and aggregation of human protein tau in a yeast model
45. O2-04-01: Combined amyloid and tau-pathology in APPV717I X taup301L double transgenic mice: Increased survival correlates with less hindbrain pathology, despite dramatic forebrain tauopathy
46. P1-015: Tau-4R suppresses precursor proliferation and promotes neuronal differentiation in the hippocampus of humanized tau knock-in/knock-out mice
47. O4–05–04: Co–expression of GSK–3β with tau–P301L in double transgenic mice dramatically increases forebrain tauopathy but decreases hindbrain pathology and rescues mortality
48. P3-277: Severe neurodegeneration is intimately related to inflammation in cdk5/p25 inducible mice
49. Improved Long-Term Potentiation and Memory in Young Tau-P301L Transgenic Mice before Onset of Hyperphosphorylation and Tauopathy
50. Changed Conformation of Mutant Tau-P301L Underlies the Moribund Tauopathy, Absent in Progressive, Nonlethal Axonopathy of Tau-4R/2N Transgenic Mice
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