Spike bursts increase amyloid-β 40/42 ratio by inducing a presenilin-1 conformational change. - sprookjes - yvandenbroek - TriplyDB

Spike bursts increase amyloid-β 40/42 ratio by inducing a presenilin-1 conformational change.

Spike bursts increase amyloid-β 40/42 ratio by inducing a presenilin-1 conformational change.

http://www.wikidata.org/entity/Q42436815

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Decreased CALM expression reduces Aβ42 to total Aβ ratio through clathrin-mediated endocytosis of γ-secretase Self-propagation of pathogenic protein aggregates in neurodegenerative diseases Identification of the novel activity-driven interaction between synaptotagmin 1 and presenilin 1 links calcium, synapse, and amyloid beta An Anti-Parkinson's Disease Drug via Targeting Adenosine A2A Receptor Enhances Amyloid-β Generation and γ-Secretase Activity Exosomes neutralize synaptic-plasticity-disrupting activity of Aβ assemblies in vivo.Structural interactions between inhibitor and substrate docking sites give insight into mechanisms of human PS1 complexes.Might cortical hyper-responsiveness in aging contribute to Alzheimer's disease?First effects of rising amyloid-β in transgenic mouse brain: synaptic transmission and gene expression.Early Cortical Changes in Gamma Oscillations in Alzheimer's Disease Biological function of Presenilin and its role in AD pathogenesis Reciprocal disruption of neuronal signaling and Aβ production mediated by extrasynaptic NMDA receptors: a downward spiral.IGF-1 Receptor Differentially Regulates Spontaneous and Evoked Transmission via Mitochondria at Hippocampal Synapses.Aβ42 and Aβ40: similarities and differences.Neuronal activity and amyloid plaque pathology: an update.Dynamic Nature of presenilin1/γ-Secretase: Implication for Alzheimer's Disease Pathogenesis.Astrocytes with previous chronic exposure to amyloid β-peptide fragment 1-40 suppress excitatory synaptic transmission.Sleep EEG Detects Epileptiform Activity in Alzheimer's Disease with High Sensitivity.Systems Pharmacology Analysis of the Amyloid Cascade after β-Secretase Inhibition Enables the Identification of an Aβ42 Oligomer Pool.Sensory Deprivation Triggers Synaptic and Intrinsic Plasticity in the Hippocampus.Intermittent hypoxia training blunts cerebrocortical presenilin 1 overexpression and amyloid-β accumulation in ethanol-withdrawn rats.The role of coupling strength and internal delay between compartments in shaping the bursting behavior of cortical neuron.Retromer in Synaptic Function and Pathology

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P2860

Spike bursts increase amyloid-β 40/42 ratio by inducing a presenilin-1 conformational change.

http://www.wikidata.org/entity/Q42436815

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2013 nî lūn-bûn

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name

Spike bursts increase amyloid- ...... nilin-1 conformational change.

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Spike bursts increase amyloid- ...... nilin-1 conformational change.

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Spike bursts increase amyloid- ...... nilin-1 conformational change.

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Spike bursts increase amyloid- ...... nilin-1 conformational change.

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Spike bursts increase amyloid- ...... nilin-1 conformational change.

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Spike bursts increase amyloid- ...... nilin-1 conformational change.

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Nature Neuroscience

P1476

Spike bursts increase amyloid- ...... nilin-1 conformational change.

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P2093

Hila Milshtein

http://www.w3.org/2001/XMLSchema#string

Hilla Fogel

http://www.w3.org/2001/XMLSchema#string

Iftach Dolev

http://www.w3.org/2001/XMLSchema#string

Inna Slutsky

http://www.w3.org/2001/XMLSchema#string

Neta Gazit

http://www.w3.org/2001/XMLSchema#string

Nils Brose

http://www.w3.org/2001/XMLSchema#string

Noa Lipstein

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Yevgeny Berdichevsky

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P2860

Neurotoxicity of Alzheimer's disease Aβ peptides is induced by small changes in the Aβ42 to Aβ40 ratio

Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks

When loss is gain: reduced presenilin proteolytic function leads to increased Abeta42/Abeta40. Talking Point on the role of presenilin mutations in Alzheimer disease

Loss-of-function presenilin mutations in Alzheimer disease. Talking Point on the role of presenilin mutations in Alzheimer disease

Distinct neuronal coding schemes in memory revealed by selective erasure of fast synchronous synaptic transmission.

Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide

Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase

Short-term synaptic plasticity

Influence of education and occupation on the incidence of Alzheimer's disease

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587-595

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10.1038/NN.3376

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5

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16

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236128298

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1048972312

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