MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
about
Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networksRAGE inhibition in microglia prevents ischemia-dependent synaptic dysfunction in an amyloid-enriched environmentEnhanced Aβ(1-40) production in endothelial cells stimulated with fibrillar Aβ(1-42)Synaptic therapy in Alzheimer's disease: a CREB-centric approach.Ablation of cellular prion protein does not ameliorate abnormal neural network activity or cognitive dysfunction in the J20 line of human amyloid precursor protein transgenic mice.Genetic deficiency of neuronal RAGE protects against AGE-induced synaptic injury.The potential mechanisms of Aβ-receptor for advanced glycation end-products interaction disrupting tight junctions of the blood-brain barrier in Alzheimer's disease.Olfactory bulb neuroproteomics reveals a chronological perturbation of survival routes and a disruption of prohibitin complex during Alzheimer's disease progressionGastrodin Protects Neural Progenitor Cells Against Amyloid β (1-42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1-42)-Injected Mice.Aβ(1-42) oligomer-induced leakage in an in vitro blood-brain barrier model is associated with up-regulation of RAGE and metalloproteinases, and down-regulation of tight junction scaffold proteins.Role of Aβ-receptor for advanced glycation endproducts interaction in oxidative stress and cytosolic phospholipase A₂ activation in astrocytes and cerebral endothelial cells.Antineuroinflammatory Effects of Modified Wu-Zi-Yan-Zong Prescription in β-Amyloid-Stimulated BV2 Microglia via the NF-κB and ERK/p38 MAPK Signaling Pathways.The role of amyloid beta clearance in cerebral amyloid angiopathy: more potential therapeutic targets.The Complexity of Sporadic Alzheimer's Disease Pathogenesis: The Role of RAGE as Therapeutic Target to Promote Neuroprotection by Inhibiting Neurovascular Dysfunction.Amyloid and Alzheimer's disease.microRNA-132/212 deficiency enhances Aβ production and senile plaque deposition in Alzheimer's disease triple transgenic mice.Esculentoside A suppresses Aβ(1-42)-induced neuroinflammation by down-regulating MAPKs pathways in vivo.Effect of α-synuclein on amyloid β-induced toxicity: relevance to Lewy body variant of Alzheimer disease.A synthetic amino acid substitution of Tyr10 in Aβ peptide sequence yields a dominant negative variant in amyloidogenesis.Mitochondrial Dysfunction Triggers Synaptic Deficits via Activation of p38 MAP Kinase Signaling in Differentiated Alzheimer's Disease Trans-Mitochondrial Cybrid Cells.Synaptic Dysfunction in Alzheimer's Disease: Aβ, Tau, and Epigenetic Alterations.Mitogen-activated protein kinase phosphatase 1 protects PC12 cells from amyloid beta-induced neurotoxicity
P2860
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P2860
MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年学术文章
@wuu
2009年学术文章
@zh-cn
2009年学术文章
@zh-hans
2009年学术文章
@zh-my
2009年学术文章
@zh-sg
2009年學術文章
@yue
2009年學術文章
@zh
2009年學術文章
@zh-hant
name
MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
@en
MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
@nl
type
label
MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
@en
MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
@nl
prefLabel
MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
@en
MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
@nl
P2860
P356
P1476
MAPK, beta-amyloid and synaptic dysfunction: the role of RAGE.
@en
P2093
Nicola Origlia
Shirley ShiDu Yan
P2860
P304
P356
10.1586/ERN.09.107
P577
2009-11-01T00:00:00Z