Suppression of eIF2α kinases alleviates Alzheimer's disease-related plasticity and memory deficits.
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Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's DiseaseThe Role of Oxidative Stress-Induced Epigenetic Alterations in Amyloid-β Production in Alzheimer's DiseaseThe unfolded protein response in neurodegenerative diseases: a neuropathological perspectiveProtein kinase R-like ER kinase and its role in endoplasmic reticulum stress-decided cell fateGenes and signaling pathways involved in memory enhancement in mutant miceHijacking PrP(c)-dependent signal transduction: when prions impair Aβ clearanceSynaptopathies: synaptic dysfunction in neurological disorders - A review from students to studentsCold-inducible proteins CIRP and RBM3, a unique couple with activities far beyond the coldReview: Modulating the unfolded protein response to prevent neurodegeneration and enhance memoryDrosophila as an In Vivo Model for Human Neurodegenerative DiseaseArginine deprivation and immune suppression in a mouse model of Alzheimer's diseaseTranslational control of auditory imprinting and structural plasticity by eIF2α.Limited effects of an eIF2αS51A allele on neurological impairments in the 5xFAD mouse model of Alzheimer's disease.Repurposed drugs targeting eIF2α-P-mediated translational repression prevent neurodegeneration in mice.Dual leucine zipper kinase-dependent PERK activation contributes to neuronal degeneration following insult.Recent Insights into the Role of Unfolded Protein Response in ER Stress in Health and Disease.Genetic reduction of mammalian target of rapamycin ameliorates Alzheimer's disease-like cognitive and pathological deficits by restoring hippocampal gene expression signatureDysregulation of Elongation Factor 1A Expression is Correlated with Synaptic Plasticity Impairments in Alzheimer's Disease.Endoplasmic reticulum stress and inflammation in the central nervous systemPERK: a novel therapeutic target for neurodegenerative diseases?Genetic inhibition of phosphorylation of the translation initiation factor eIF2α does not block Aβ-dependent elevation of BACE1 and APP levels or reduce amyloid pathology in a mouse model of Alzheimer's disease.Role of Endoplasmic Reticulum Stress in Learning and Memory Impairment and Alzheimer's Disease-Like Neuropathology in the PS19 and APPSwe Mouse Models of Tauopathy and Amyloidosis.PERK mediates eIF2α phosphorylation responsible for BACE1 elevation, CREB dysfunction and neurodegeneration in a mouse model of Alzheimer's disease.Inhibition of AMP-activated protein kinase signaling alleviates impairments in hippocampal synaptic plasticity induced by amyloid β.A new PERKspective on neurodegeneration.Transcriptional and epigenetic substrates of methamphetamine addiction and withdrawal: evidence from a long-access self-administration model in the rat.Dysregulation of RNA Binding Protein Aggregation in Neurodegenerative Disorders.P2Y receptors in Alzheimer's disease.Alzheimer-associated Aβ oligomers impact the central nervous system to induce peripheral metabolic deregulation.Somatostatin, neuronal vulnerability and behavioral emotionality.Novel VCP modulators mitigate major pathologies of rd10, a mouse model of retinitis pigmentosa.Actin dynamics tune the integrated stress response by regulating eukaryotic initiation factor 2α dephosphorylation.Pharmacological dimerization and activation of the exchange factor eIF2B antagonizes the integrated stress response.Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer's diseaseUnfolded Protein Response and PERK Kinase as a New Therapeutic Target in the Pathogenesis of Alzheimer's DiseaseReprogramming patient-derived cells to study the epilepsiesImpaired protein translation in Drosophila models for Charcot-Marie-Tooth neuropathy caused by mutant tRNA synthetasesReducing Ribosomal Protein S6 Kinase 1 Expression Improves Spatial Memory and Synaptic Plasticity in a Mouse Model of Alzheimer's Disease.PERK inhibition prevents tau-mediated neurodegeneration in a mouse model of frontotemporal dementia.Paradoxical Sensitivity to an Integrated Stress Response Blocking Mutation in Vanishing White Matter Cells.
P2860
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P2860
Suppression of eIF2α kinases alleviates Alzheimer's disease-related plasticity and memory deficits.
description
2013 nî lūn-bûn
@nan
2013 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
name
Suppression of eIF2α kinases a ...... lasticity and memory deficits.
@ast
Suppression of eIF2α kinases a ...... lasticity and memory deficits.
@en
type
label
Suppression of eIF2α kinases a ...... lasticity and memory deficits.
@ast
Suppression of eIF2α kinases a ...... lasticity and memory deficits.
@en
prefLabel
Suppression of eIF2α kinases a ...... lasticity and memory deficits.
@ast
Suppression of eIF2α kinases a ...... lasticity and memory deficits.
@en
P2093
P2860
P356
P1433
P1476
Suppression of eIF2α kinases a ...... lasticity and memory deficits.
@en
P2093
Alyse J Wexler
Clarisse Bourbon
Douglas R Cavener
Eric Klann
Evelina Gatti
Mimi A Trinh
Philippe Pierre
P2860
P2888
P304
P356
10.1038/NN.3486
P407
P577
2013-08-11T00:00:00Z
P5875
P6179
1005320994