Non-selective NSAIDs improve the amyloid-β-mediated suppression of memory and synaptic plasticity.
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Acetylated tau in Alzheimer's disease: An instigator of synaptic dysfunction underlying memory loss: Increased levels of acetylated tau blocks the postsynaptic signaling required for plasticity and promotes memory deficits associated with tauopathy.Cyclooxygenase-1 as a Potential Therapeutic Target for Seizure Suppression: Evidences from Zebrafish Pentylenetetrazole-Seizure Model.Galantamine improves cognition, hippocampal inflammation, and synaptic plasticity impairments induced by lipopolysaccharide in mice.Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer's Disease.Mitogen-activated protein kinase phosphatase 1 protects PC12 cells from amyloid beta-induced neurotoxicity
P2860
Non-selective NSAIDs improve the amyloid-β-mediated suppression of memory and synaptic plasticity.
description
2015 nî lūn-bûn
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2015年の論文
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2015年学术文章
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2015年学术文章
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2015年学术文章
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2015年学术文章
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2015年学术文章
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2015年學術文章
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name
Non-selective NSAIDs improve t ...... emory and synaptic plasticity.
@en
Non-selective NSAIDs improve t ...... emory and synaptic plasticity.
@nl
type
label
Non-selective NSAIDs improve t ...... emory and synaptic plasticity.
@en
Non-selective NSAIDs improve t ...... emory and synaptic plasticity.
@nl
prefLabel
Non-selective NSAIDs improve t ...... emory and synaptic plasticity.
@en
Non-selective NSAIDs improve t ...... emory and synaptic plasticity.
@nl
P2093
P50
P1476
Non-selective NSAIDs improve t ...... memory and synaptic plasticity
@en
P2093
Jafar Doost Mohammadpour
Mahyar Janahmadi
Narges Hosseinmardi
P356
10.1016/J.PBB.2015.02.012
P407
P577
2015-02-17T00:00:00Z