Pages that link to "Q41903311"
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The following pages link to Amyloid-β nanotubes are associated with prion protein-dependent synaptotoxicity. (Q41903311):
Displaying 47 items.
- Amyloid-β Receptors: The Good, the Bad, and the Prion Protein (Q26771532) (← links)
- Alzheimer's Disease: Mechanism and Approach to Cell Therapy (Q26778149) (← links)
- Assessing the causes and consequences of co-polymerization in amyloid formation (Q26824195) (← links)
- Integration of multiscale dendritic spine structure and function data into systems biology models (Q27003132) (← links)
- Hijacking PrP(c)-dependent signal transduction: when prions impair Aβ clearance (Q27009790) (← links)
- Interaction between prion protein and Aβ amyloid fibrils revisited (Q27013909) (← links)
- EPPS rescues hippocampus-dependent cognitive deficits in APP/PS1 mice by disaggregation of amyloid-β oligomers and plaques (Q27316634) (← links)
- Amyloid β Protein and Alzheimer's Disease: When Computer Simulations Complement Experimental Studies (Q33893017) (← links)
- N-terminal domain of prion protein directs its oligomeric association (Q34170632) (← links)
- Cellular prion protein and NMDA receptor modulation: protecting against excitotoxicity (Q34391341) (← links)
- mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo (Q35160799) (← links)
- Single-molecule imaging reveals that small amyloid-β1-42 oligomers interact with the cellular prion protein (PrP(C)) (Q35211687) (← links)
- Amyloid polymorphism: structural basis and neurobiological relevance (Q35586308) (← links)
- Therapeutic potential of mGluR5 targeting in Alzheimer's disease (Q35698522) (← links)
- Prion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models. (Q35837187) (← links)
- A Neuronal Culture System to Detect Prion Synaptotoxicity (Q36030390) (← links)
- Electrostatically-guided inhibition of Curli amyloid nucleation by the CsgC-like family of chaperones (Q36819800) (← links)
- Metabotropic glutamate receptor 5 couples cellular prion protein to intracellular signalling in Alzheimer's disease (Q36824513) (← links)
- Soluble prion protein and its N-terminal fragment prevent impairment of synaptic plasticity by Aβ oligomers: Implications for novel therapeutic strategy in Alzheimer's disease (Q36880081) (← links)
- The Anti-Prion Antibody 15B3 Detects Toxic Amyloid-β Oligomers (Q37300268) (← links)
- Decoding the function of the N-terminal tail of the cellular prion protein to inspire novel therapeutic avenues for neurodegenerative diseases (Q38279734) (← links)
- The Unexposed Secrets of Prion Protein Oligomers (Q38396095) (← links)
- Cross-interactions between the Alzheimer Disease Amyloid-β Peptide and Other Amyloid Proteins: A Further Aspect of the Amyloid Cascade Hypothesis (Q38871578) (← links)
- Binding Sites for Amyloid-β Oligomers and Synaptic Toxicity (Q39035492) (← links)
- Heme oxygenase-1 protects against Alzheimer's amyloid-β(1-42)-induced toxicity via carbon monoxide production (Q41697205) (← links)
- Intracellular oligomeric amyloid-beta rapidly regulates GluA1 subunit of AMPA receptor in the hippocampus. (Q41975566) (← links)
- Identification of a Compound That Disrupts Binding of Amyloid-β to the Prion Protein Using a Novel Fluorescence-based Assay (Q42350107) (← links)
- Cellular prion protein targets amyloid-β fibril ends via its C-terminal domain to prevent elongation (Q46316131) (← links)
- Non-Fibrillar Oligomeric Amyloid-β within Synapses (Q46538110) (← links)
- Soluble Aβ aggregates can inhibit prion propagation. (Q47104343) (← links)
- Amyloid Beta Peptides Block New Synapse Assembly by Nogo Receptor-Mediated Inhibition of T-Type Calcium Channels (Q47661801) (← links)
- Kalirin reduction rescues psychosis-associated behavioral deficits in APPswe/PSEN1dE9 transgenic mice (Q47771892) (← links)
- Opposite in vivo effects of agents that stimulate or inhibit the glutamate/cysteine exchanger system xc- on the inhibition of hippocampal LTP by Aß. (Q48475079) (← links)
- Synaptotoxic Signaling by Amyloid Beta Oligomers in Alzheimer's Disease Through Prion Protein and mGluR5. (Q50138252) (← links)
- Single molecule study of initial structural features on the amyloidosis process (Q51411240) (← links)
- Cannabidiol Reverses Deficits in Hippocampal LTP in a Model of Alzheimer's Disease. (Q52637940) (← links)
- A new era for understanding amyloid structures and disease (Q57787227) (← links)
- Protein folding in the cell, from atom to organism (Q57854068) (← links)
- Prions activate a p38 MAPK synaptotoxic signaling pathway (Q58712857) (← links)
- Structural Determinants of the Prion Protein N-Terminus and Its Adducts with Copper Ions (Q61456169) (← links)
- Prion protein stabilizes amyloid-β (Aβ) oligomers and enhances Aβ neurotoxicity in a Drosophila model of Alzheimer's disease (Q89055701) (← links)
- A mechanistic hypothesis for the impairment of synaptic plasticity by soluble Aβ oligomers from Alzheimer's brain (Q90375051) (← links)
- PrP is a central player in toxicity mediated by soluble aggregates of neurodegeneration-causing proteins (Q92103662) (← links)
- Cellular Prion Protein as a Receptor of Toxic Amyloid-β42 Oligomers Is Important for Alzheimer's Disease (Q92649273) (← links)
- "Dual Disease" TgAD/GSS mice exhibit enhanced Alzheimer's disease pathology and reveal PrPC-dependent secretion of Aβ (Q92690994) (← links)
- Molecular interactions between monoclonal oligomer-specific antibody 5E3 and its amyloid beta cognates (Q95943213) (← links)
- Sleep is bi-directionally modified by amyloid beta oligomers (Q97523509) (← links)