BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer's disease
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Herpes Simplex Virus Type 1 and Other Pathogens are Key Causative Factors in Sporadic Alzheimer's DiseaseThe normal and pathologic roles of the Alzheimer's β-secretase, BACE1BMS-708163 and Nilotinib restore synaptic dysfunction in human embryonic stem cell-derived Alzheimer's disease modelsAn Overview of the Protective Effects of Chitosan and Acetylated Chitosan Oligosaccharides against Neuronal Disorders.Elevated Aβ42 in aged, non-demented individuals with cerebral atherosclerosis.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.Function, therapeutic potential and cell biology of BACE proteases: current status and future prospects.Differential spatio-temporal regulation of MMPs in the 5xFAD mouse model of Alzheimer's disease: evidence for a pro-amyloidogenic role of MT1-MMP.Deficiency in LRP6-mediated Wnt signaling contributes to synaptic abnormalities and amyloid pathology in Alzheimer's disease.Effect of the CALHM1 G330D and R154H human variants on the control of cytosolic Ca2+ and Aβ levels.The γ-secretase complex: from structure to function.Mild oxidative stress induces redistribution of BACE1 in non-apoptotic conditions and promotes the amyloidogenic processing of Alzheimer's disease amyloid precursor proteinAxonal and Schwann cell BACE1 is equally required for remyelination of peripheral nerves.Edaravone alleviates Alzheimer's disease-type pathologies and cognitive deficitsAmyloid-β Peptide Exacerbates the Memory Deficit Caused by Amyloid Precursor Protein Loss-of-Function in Drosophila.Future Therapeutics in Alzheimer's Disease: Development Status of BACE Inhibitors.α-Synuclein increases β-amyloid secretion by promoting β-/γ-secretase processing of APP.Deficiency of Neuronal p38α MAPK Attenuates Amyloid Pathology in Alzheimer Disease Mouse and Cell Models through Facilitating Lysosomal Degradation of BACE1.miR-186 is decreased in aged brain and suppresses BACE1 expressionSyntaxin 5 Overexpression and β-Amyloid 1-42 Accumulation in Endoplasmic Reticulum of Hippocampal Cells in Rat Brain Induced by Ozone ExposureAlzheimer's Disease: Assessing the Role of Spirochetes, Biofilms, the Immune System, and Amyloid-β with Regard to Potential Treatment and Prevention.Transcriptional regulation and its misregulation in Alzheimer's disease.High glucose upregulates BACE1-mediated Aβ production through ROS-dependent HIF-1α and LXRα/ABCA1-regulated lipid raft reorganization in SK-N-MC cells.Disturbed Matrix Metalloproteinase Pathway in Both Age-Related Macular Degeneration and Alzheimer's DiseaseCan BACE1 inhibition mitigate early axonal pathology in neurological diseases?BACE1 as a therapeutic target in Alzheimer's disease: rationale and current status.M1 muscarinic acetylcholine receptor in Alzheimer's diseaseRyanodine receptors: physiological function and deregulation in Alzheimer disease.BACE1 inhibitor drugs in clinical trials for Alzheimer's disease.Cannabinoids for the Treatment of Agitation and Aggression in Alzheimer's Disease.Multiple mechanisms of iron-induced amyloid beta-peptide accumulation in SHSY5Y cells: protective action of negletein.Enhanced amyloidogenic processing of amyloid precursor protein and cell death under prolonged endoplasmic reticulum stress in brain endothelial cells.Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in Alzheimer's disease and Parkinson's diseaseThe emerging role of alternative splicing in senescence and aging.Early Growth Response 1 (Egr-1) Is a Transcriptional Activator of β-Secretase 1 (BACE-1) in the BrainAβ42 oligomers modulate β-secretase through an XBP-1s-dependent pathway involving HRD1.Molecular neurodegeneration: basic biology and disease pathways.Mitochondrial dysfunction in the APP/PSEN1 mouse model of Alzheimer's disease and a novel protective role for ascorbate.BACE1 elevation engendered by GGA3 deletion increases β-amyloid pathology in association with APP elevation and decreased CHL1 processing in 5XFAD mice.Chronic Sleep Restriction Induces Cognitive Deficits and Cortical Beta-Amyloid Deposition in Mice via BACE1-Antisense Activation.
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P2860
BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer's disease
description
2012 nî lūn-bûn
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2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
2012年學術文章
@zh
2012年學術文章
@zh-hant
name
BACE1 is at the crossroad of a ...... duction in Alzheimer's disease
@ast
BACE1 is at the crossroad of a ...... duction in Alzheimer's disease
@en
type
label
BACE1 is at the crossroad of a ...... duction in Alzheimer's disease
@ast
BACE1 is at the crossroad of a ...... duction in Alzheimer's disease
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prefLabel
BACE1 is at the crossroad of a ...... duction in Alzheimer's disease
@ast
BACE1 is at the crossroad of a ...... duction in Alzheimer's disease
@en
P2860
P921
P356
P1476
BACE1 is at the crossroad of a ...... duction in Alzheimer's disease
@en
P2860
P2888
P356
10.1186/1750-1326-7-52
P5008
P577
2012-10-05T00:00:00Z
P5875
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1033733299