Inhibition of GSK-3 ameliorates Abeta pathology in an adult-onset Drosophila model of Alzheimer's disease.
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Therapeutic potential of mood stabilizers lithium and valproic acid: beyond bipolar disorderThe roles of lipid and glucose metabolism in modulation of β-amyloid, tau, and neurodegeneration in the pathogenesis of Alzheimer diseaseLoss of Polo ameliorates APP-induced Alzheimer's disease-like symptoms in DrosophilaNebula/DSCR1 upregulation delays neurodegeneration and protects against APP-induced axonal transport defects by restoring calcineurin and GSK-3β signalingModeling the complex pathology of Alzheimer's disease in DrosophilaAgeing increases vulnerability to aβ42 toxicity in DrosophilaLithium suppresses Aβ pathology by inhibiting translation in an adult Drosophila model of Alzheimer's diseaseOligomer-targeting with a conformational antibody fragment promotes toxicity in Aβ-expressing flies.Loss of axonal mitochondria promotes tau-mediated neurodegeneration and Alzheimer's disease-related tau phosphorylation via PAR-1.Lack of evidence of the interaction of the Aβ peptide with the Wnt signaling cascade in Drosophila models of Alzheimer's diseaseA Drosophila model of FUS-related neurodegeneration reveals genetic interaction between FUS and TDP-43.Parallel profiling of fission yeast deletion mutants for proliferation and for lifespan during long-term quiescence.GSK-3 in Neurodegenerative Diseases.GSK-3 as a Target for Lithium-Induced Neuroprotection Against Excitotoxicity in Neuronal Cultures and Animal Models of Ischemic Stroke.A commonly used Drosophila model of Alzheimer's disease generates an aberrant species of amyloid-β with an additional N-terminal glutamine residue.Manipulations of amyloid precursor protein cleavage disrupt the circadian clock in aging Drosophila.Functional genomic screen and network analysis reveal novel modifiers of tauopathy dissociated from tau phosphorylation.GSK3β inhibition promotes synaptogenesis in Drosophila and mammalian neurons.Amyloid-β Peptide Exacerbates the Memory Deficit Caused by Amyloid Precursor Protein Loss-of-Function in Drosophila.Aβ43 is neurotoxic and primes aggregation of Aβ40 in vivo.Bidirectional Regulation of Amyloid Precursor Protein-Induced Memory Defects by Nebula/DSCR1: A Protein Upregulated in Alzheimer's Disease and Down SyndromeStabilization of Microtubule-Unbound Tau via Tau Phosphorylation at Ser262/356 by Par-1/MARK Contributes to Augmentation of AD-Related Phosphorylation and Aβ42-Induced Tau Toxicity.Herpes Simplex Virus type-1 infection induces synaptic dysfunction in cultured cortical neurons via GSK-3 activation and intraneuronal amyloid-β protein accumulationDirect Keap1-Nrf2 disruption as a potential therapeutic target for Alzheimer's disease.Lack of miRNA Misregulation at Early Pathological Stages in Drosophila Neurodegenerative Disease Models.Presynaptic Aβ40 prevents synapse addition in the adult Drosophila neuromuscular junction.Deletion of endogenous Tau proteins is not detrimental in Drosophila.An exploration of the potential mechanisms and translational potential of five medicinal plants for applications in Alzheimer's disease.Increased Glucose Transport into Neurons Rescues Aβ Toxicity in Drosophila.Amyloid beta-induced glycogen synthase kinase 3β phosphorylated VDAC1 in Alzheimer's disease: implications for synaptic dysfunction and neuronal damagepGluAβ increases accumulation of Aβ in vivo and exacerbates its toxicity.A holidic medium for Drosophila melanogaster.Traditional Chinese Medicine Huannao Yicong Decoction Extract Decreases Tau Hyperphosphorylation in the Brain of Alzheimer's Disease Model Rats Induced by Aβ1-42.Six psychotropics for pre-symptomatic & early Alzheimer's (MCI), Parkinson's, and Huntington's disease modification.Multiple faces of dynamin-related protein 1 and its role in Alzheimer's disease pathogenesisLithium in neuropsychiatry: a 2010 update.The power and richness of modelling tauopathies in Drosophila.Interaction between pathogenic proteins in neurodegenerative disorders.Modelling tauopathies in Drosophila: insights from the fruit fly.Understanding the relationship between GSK-3 and Alzheimer's disease: a focus on how GSK-3 can modulate synaptic plasticity processes.
P2860
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P2860
Inhibition of GSK-3 ameliorates Abeta pathology in an adult-onset Drosophila model of Alzheimer's disease.
description
2010 nî lūn-bûn
@nan
2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Inhibition of GSK-3 ameliorate ...... model of Alzheimer's disease.
@ast
Inhibition of GSK-3 ameliorate ...... model of Alzheimer's disease.
@en
type
label
Inhibition of GSK-3 ameliorate ...... model of Alzheimer's disease.
@ast
Inhibition of GSK-3 ameliorate ...... model of Alzheimer's disease.
@en
prefLabel
Inhibition of GSK-3 ameliorate ...... model of Alzheimer's disease.
@ast
Inhibition of GSK-3 ameliorate ...... model of Alzheimer's disease.
@en
P2093
P2860
P50
P921
P1433
P1476
Inhibition of GSK-3 ameliorate ...... model of Alzheimer's disease.
@en
P2093
Carina Gandy
Hrvoje Augustin
Iain Rogers
Marcus J Allen
Oyinkan Sofola
P2860
P304
P356
10.1371/JOURNAL.PGEN.1001087
P577
2010-09-02T00:00:00Z