789 results on '"Selkoe, Dennis J"'
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2. Author Correction: Generation of G51D and 3D mice reveals decreased α-synuclein tetramer-monomer ratios promote Parkinson’s disease phenotypes
3. Generation of G51D and 3D mice reveals decreased α-synuclein tetramer-monomer ratios promote Parkinson’s disease phenotypes
4. Dynamic physiological α-synuclein S129 phosphorylation is driven by neuronal activity
5. Wild-type GBA1 increases the α-synuclein tetramer–monomer ratio, reduces lipid-rich aggregates, and attenuates motor and cognitive deficits in mice
6. A Brain-Penetrant Stearoyl-CoA Desaturase Inhibitor Reverses α-Synuclein Toxicity
7. Parkinson-causing mutations in LRRK2 impair the physiological tetramerization of endogenous α-synuclein in human neurons
8. β2-Adrenoreceptor is a regulator of the α-synuclein gene driving risk of Parkinson’s disease
9. Fluorescent Analogue of Batimastat Enables Imaging of alpha-Secretase in Living Cells
10. Genomic DISC1 Disruption in hiPSCs Alters Wnt Signaling and Neural Cell Fate
11. Correction to: A Brain-Penetrant Stearoyl-CoA Desaturase Inhibitor Reverses α-Synuclein Toxicity
12. Uncovering elevated tau TPP motif phosphorylation in the brain of Alzheimer's disease patients.
13. Soluble Aβ Oligomers Impair Dipolar Heterodendritic Plasticity by Activation of mGluR in the Hippocampal CA1 Region
14. Plasma N-terminal tau fragment levels predict future cognitive decline and neurodegeneration in healthy elderly individuals
15. Abundant Aβ fibrils in ultracentrifugal supernatants of aqueous extracts from Alzheimer’s disease brains
16. The Parkinson-Associated Toxin Paraquat Shifts Physiological α-Synuclein Tetramers toward Monomers That Can Be Calpain-Truncated and Form Oligomers
17. γ-Secretase Is a Membrane Protein Complex Comprised of Presenilin, Nicastrin, Aph-1, and Pen-2
18. Insulin-Degrading Enzyme Regulates the Levels of Insulin, Amyloid β-Protein, and the β-Amyloid Precursor Protein Intracellular Domain in vivo
19. The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
20. Activity-Dependent Isolation of the Presenilin- γ-Secretase Complex Reveals Nicastrin and a γ Substrate
21. Dynamics of plasma biomarkers in Down syndrome: the relative levels of Aβ42 decrease with age, whereas NT1 tau and NfL increase
22. Immune Hyporesponsiveness to Amyloid β-Peptide in Amyloid Precursor Protein Transgenic Mice: Implications for the Pathogenesis and Treatment of Alzheimer's Disease
23. α-Synuclein Occurs in Lipid-Rich High Molecular Weight Complexes, Binds Fatty Acids, and Shows Homology to the Fatty Acid-Binding Proteins
24. Ubiquitination of a New Form of α-Synuclein by Parkin from Human Brain: Implications for Parkinson's Disease
25. Dynamic reversibility of α‐synuclein serine‐129 phosphorylation is impaired in synucleinopathy models.
26. Presenilin Complexes with the C-Terminal Fragments of Amyloid Precursor Protein at the Sites of Amyloid β -Protein Generation
27. Kinetics of Amyloid β-Protein Degradation Determined by Novel Fluorescence- and Fluorescence Polarization-based Assays*
28. Kinetics of amyloid beta-protein degradation determined by novel fluorescence- and fluorescence polarization-based assays.
29. Interaction between Amyloid Precursor Protein and Presenilins in Mammalian Cells: Implications for the Pathogenesis of Alzheimer Disease
30. Proteolytic Processing of the Alzheimer Disease-Associated Presenilin-1 Generates an in vivo Substrate for Protein Kinase C
31. In vitro studies of amyloid β-protein fibril assembly and toxicity provide clues to the aetiology of Flemish variant (Ala692→Gly) Alzheimer's disease
32. Evidence that the 42- and 40-Amino Acid Forms of Amyloid β Protein are Generated from the β -amyloid Precursor Protein by Different Protease Activities
33. A de novo designed helix-turn-helix peptide forms nontoxic amyloid fibrils
34. An improved method of preparing the amyloid β-protein for fibrillogenesis and neurotoxicity experiments
35. Caspase-1 clipping causes complications for α-synuclein
36. Nicastrin functions to sterically hinder γ-secretase–substrate interactions driven by substrate transmembrane domain
37. Plasma NT1-tau and Aβ (42) correlate with age and cognitive function in two large Down syndrome cohorts
38. Protofibrillar Intermediates of Amyloid β-Protein Induce Acute Electrophysiological Changes and Progressive Neurotoxicity in Cortical Neurons
39. Amyloid β-Protein Fibrillogenesis STRUCTURE AND BIOLOGICAL ACTIVITY OF PROTOFIBRILLAR INTERMEDIATES*
40. Heparin-binding Properties of the Amyloidogenic Peptides Aβ and Amylin DEPENDENCE ON AGGREGATION STATE AND INHIBITION BY CONGO RED*
41. Enriched environment enhances β‐adrenergic signaling to prevent microglia inflammation by amyloid‐β
42. Decoding the synaptic dysfunction of bioactive human AD brain soluble Aβ to inspire novel therapeutic avenues for Alzheimer’s disease
43. Aβ oligomers from human brain impair mossy fiber LTP in CA3 of hippocampus, but activating cAMP-PKA and cGMP-PKG prevents this
44. The Search for an Amyloid Solution
45. Alzheimer's Disease Is a Synaptic Failure
46. Presenilin, Notch, and the Genesis and Treatment of Alzheimer's Disease
47. Alzheimer disease and aducanumab: adjusting our approach
48. In Search of γ -Secretase: Presenilin at the Cutting Edge
49. The amyloid hypothesis of Alzheimer's disease at 25 years
50. Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration
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