Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β. - Wikidata - wikimedia - TriplyDB

Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β.

Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β.

http://www.wikidata.org/entity/Q50524206

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Caspases in synaptic plasticity Alzheimer mechanisms and therapeutic strategies Cell biology in neuroscience: Death of developing neurons: new insights and implications for connectivity Evidence for irreversible inhibition of glycogen synthase kinase-3β by tideglusib Synapses and Alzheimer's disease Amyloid-β-Induced Dysregulation of AMPA Receptor Trafficking Role of physical and mental training in brain network configuration Food for thought: the role of appetitive peptides in age-related cognitive decline Interactions between mitochondria and the transcription factor myocyte enhancer factor 2 (MEF2) regulate neuronal structural and functional plasticity and metaplasticity Synaptic dysfunction and septin protein family members in neurodegenerative diseases Intraneuronal Aβ accumulation induces hippocampal neuron hyperexcitability through A-type K(+) current inhibition mediated by activation of caspases and GSK-3.Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss Microtubule-associated protein tau is essential for long-term depression in the hippocampus Alzheimer's therapeutics targeting amyloid beta 1-42 oligomers II: Sigma-2/PGRMC1 receptors mediate Abeta 42 oligomer binding and synaptotoxicity Caspase-3 activation as a bifurcation point between plasticity and cell death.Growth factors in synaptic function.Inhibition of GSK3β-mediated BACE1 expression reduces Alzheimer-associated phenotypes.Andrographolide reduces cognitive impairment in young and mature AβPPswe/PS-1 mice Cyclin Y inhibits plasticity-induced AMPA receptor exocytosis and LTP.Memory and synaptic plasticity are impaired by dysregulated hippocampal O-GlcNAcylation.Wild-Type, but Not Mutant N296H, Human Tau Restores Aβ-Mediated Inhibition of LTP in Tau-/- mice.Cholesterol in the Pathogenesis of Alzheimer's, Parkinson's Diseases and Autism: Link to Synaptic Dysfunction Computational identification of potential multitarget treatments for ameliorating the adverse effects of amyloid-β on synaptic plasticity Caspase inhibition in select olfactory neurons restores innate attraction behavior in aged Drosophila.Brain Na(+), K(+)-ATPase Activity In Aging and Disease.Dietary and behavioral interventions protect against age related activation of caspase cascades in the canine brain.Inhibition of AMP-activated protein kinase signaling alleviates impairments in hippocampal synaptic plasticity induced by amyloid β.More than cholesterol transporters: lipoprotein receptors in CNS function and neurodegeneration Models of β-amyloid induced Tau-pathology: the long and "folded" road to understand the mechanism.Neuritin can normalize neural deficits of Alzheimer's disease.Mechanism of neuromuscular dysfunction in Krabbe disease.Brain-derived neurotrophic factor ameliorates learning deficits in a rat model of Alzheimer's disease induced by aβ1-42 (R)-(+)-α-lipoic acid protected NG108-15 cells against H₂O₂-induced cell death through PI3K-Akt/GSK-3β pathway and suppression of NF-κβ-cytokines.Caspase-2 is required for dendritic spine and behavioural alterations in J20 APP transgenic mice.The Ca(2+) channel inhibitor 2-APB reverses β-amyloid-induced LTP deficit in hippocampus by blocking BAX and caspase-3 hyperactivation Tau reduction prevents Aβ-induced axonal transport deficits by blocking activation of GSK3β.Amyloid β: linking synaptic plasticity failure to memory disruption in Alzheimer's disease Mechanism of Oxidative Stress and Synapse Dysfunction in the Pathogenesis of Alzheimer's Disease: Understanding the Therapeutics Strategies A pivotal role of GSK-3 in synaptic plasticity.

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Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β.

http://www.wikidata.org/entity/Q50524206

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2011 nî lūn-bûn

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name

Aβ(1-42) inhibition of LTP is ...... ng caspase-3, Akt1 and GSK-3β.

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Aβ(1-42) inhibition of LTP is ...... ng caspase-3, Akt1 and GSK-3β.

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type

label

Aβ(1-42) inhibition of LTP is ...... ng caspase-3, Akt1 and GSK-3β.

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Aβ(1-42) inhibition of LTP is ...... ng caspase-3, Akt1 and GSK-3β.

@nl

prefLabel

Aβ(1-42) inhibition of LTP is ...... ng caspase-3, Akt1 and GSK-3β.

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Aβ(1-42) inhibition of LTP is ...... ng caspase-3, Akt1 and GSK-3β.

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Nature Neuroscience

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Aβ(1-42) inhibition of LTP is ...... ng caspase-3, Akt1 and GSK-3β.

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Bryony Dickinson

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Gilles Bru-Mercier

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Graham Collingridge

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Jihoon Jo

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Kimberly Moore Olsen

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Kwangwook Cho

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Morgan Sheng

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Sarah Scullion

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Shih-Ching Lo

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Talitha L Kerrigan

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Pathways towards and away from Alzheimer's disease

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

Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

The selectivity of protein kinase inhibitors: a further update

Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake

Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo

GSK-3alpha regulates production of Alzheimer's disease amyloid-beta peptides

LTP inhibits LTD in the hippocampus via regulation of GSK3beta

Multiple caspases are involved in beta-amyloid-induced neuronal apoptosis

AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss

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545-547

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10.1038/NN.2785

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5

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14

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Daniel J. Whitcomb

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2011-03-27T00:00:00Z

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50868360

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21441921

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