1,769 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. The advent of Alzheimer treatments will change the trajectory of human aging
5. Activation of β2-adrenergic receptors prevents AD-type synaptotoxicity via epigenetic mechanisms
6. γ-Secretase activity, clinical features, and biomarkers of autosomal dominant Alzheimer's disease: cross-sectional and longitudinal analysis of the Dominantly Inherited Alzheimer Network observational study (DIAN-OBS)
7. Dynamic physiological α-synuclein S129 phosphorylation is driven by neuronal activity
8. Soluble oligomers or insoluble fibrils? Scientific commentary on “Tau seeding and spreading in vivo is supported by both AD-derived fibrillar and oligomeric tau”
9. Wild-type GBA1 increases the α-synuclein tetramer–monomer ratio, reduces lipid-rich aggregates, and attenuates motor and cognitive deficits in mice
10. A Brain-Penetrant Stearoyl-CoA Desaturase Inhibitor Reverses α-Synuclein Toxicity
11. Parkinson-causing mutations in LRRK2 impair the physiological tetramerization of endogenous α-synuclein in human neurons
12. Lecanemab and Vascular-Amyloid Deposition in Brains of People With Down Syndrome.
13. β2-Adrenoreceptor is a regulator of the α-synuclein gene driving risk of Parkinson’s disease
14. Potential human transmission of amyloid β pathology: surveillance and risks
15. Fluorescent Analogue of Batimastat Enables Imaging of alpha-Secretase in Living Cells
16. Comparing the effectiveness of a brief observational study protocol versus a telephone call for Alzheimer’s disease prevention trial prescreening
17. A brief questionnaire of self‐reported cognitive decline predicts MMSE and study partner QDRS: findings from the Davis Memory and Aging Cohort at Mass General Brigham
18. Utilizing low‐volume PBMC samples from Alzheimer’s disease clinical research cohorts for immune cell RNA‐sequencing
19. Genomic DISC1 Disruption in hiPSCs Alters Wnt Signaling and Neural Cell Fate
20. Multiple BACE1 inhibitors abnormally increase the BACE1 protein level in neurons by prolonging its half-life
21. Learnings about the complexity of extracellular tau aid development of a blood-based screen for Alzheimer's disease
22. Correction to: A Brain-Penetrant Stearoyl-CoA Desaturase Inhibitor Reverses α-Synuclein Toxicity
23. Uncovering elevated tau TPP motif phosphorylation in the brain of Alzheimer's disease patients.
24. Soluble Aβ Oligomers Impair Dipolar Heterodendritic Plasticity by Activation of mGluR in the Hippocampal CA1 Region
25. Plasma N-terminal tau fragment levels predict future cognitive decline and neurodegeneration in healthy elderly individuals
26. Abundant Aβ fibrils in ultracentrifugal supernatants of aqueous extracts from Alzheimer’s disease brains
27. The Parkinson-Associated Toxin Paraquat Shifts Physiological α-Synuclein Tetramers toward Monomers That Can Be Calpain-Truncated and Form Oligomers
28. γ-Secretase Is a Membrane Protein Complex Comprised of Presenilin, Nicastrin, Aph-1, and Pen-2
29. Insulin-Degrading Enzyme Regulates the Levels of Insulin, Amyloid β-Protein, and the β-Amyloid Precursor Protein Intracellular Domain in vivo
30. The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics
31. Activity-Dependent Isolation of the Presenilin- γ-Secretase Complex Reveals Nicastrin and a γ Substrate
32. Dynamics of plasma biomarkers in Down syndrome: the relative levels of Aβ42 decrease with age, whereas NT1 tau and NfL increase
33. Immune Hyporesponsiveness to Amyloid β-Peptide in Amyloid Precursor Protein Transgenic Mice: Implications for the Pathogenesis and Treatment of Alzheimer's Disease
34. α-Synuclein Occurs in Lipid-Rich High Molecular Weight Complexes, Binds Fatty Acids, and Shows Homology to the Fatty Acid-Binding Proteins
35. Ubiquitination of a New Form of α-Synuclein by Parkin from Human Brain: Implications for Parkinson's Disease
36. Dynamic reversibility of α‐synuclein serine‐129 phosphorylation is impaired in synucleinopathy models.
37. Plasma NT1‐tau and Aβ42 correlate with age and cognitive function in two large Down syndrome cohorts.
38. Presenilin Complexes with the C-Terminal Fragments of Amyloid Precursor Protein at the Sites of Amyloid β -Protein Generation
39. Kinetics of Amyloid β-Protein Degradation Determined by Novel Fluorescence- and Fluorescence Polarization-based Assays*
40. Kinetics of amyloid beta-protein degradation determined by novel fluorescence- and fluorescence polarization-based assays.
41. MicroRNA-132 provides neuroprotection for tauopathies via multiple signaling pathways
42. Interaction between Amyloid Precursor Protein and Presenilins in Mammalian Cells: Implications for the Pathogenesis of Alzheimer Disease
43. Moving beyond amyloid and tau to capture the biological heterogeneity of Alzheimer’s disease
44. Proteolytic Processing of the Alzheimer Disease-Associated Presenilin-1 Generates an in vivo Substrate for Protein Kinase C
45. Palmitoylation of the Parkinson’s disease–associated protein synaptotagmin-11 links its turnover to α-synuclein homeostasis
46. In vitro studies of amyloid β-protein fibril assembly and toxicity provide clues to the aetiology of Flemish variant (Ala692→Gly) Alzheimer's disease
47. 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
48. A de novo designed helix-turn-helix peptide forms nontoxic amyloid fibrils
49. An improved method of preparing the amyloid β-protein for fibrillogenesis and neurotoxicity experiments
50. Caspase-1 clipping causes complications for α-synuclein
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