Neurotoxic mechanisms caused by the Alzheimer's disease-linked Swedish amyloid precursor protein mutation: oxidative stress, caspases, and the JNK pathway.
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Comprehensive analysis of APOE and selected proximate markers for late-onset Alzheimer's disease: patterns of linkage disequilibrium and disease/marker association.c-Jun N-terminal Kinase (JNK) Signaling as a Therapeutic Target for Alzheimer's DiseaseRole of methylglyoxal in Alzheimer's diseaseBattery of behavioral tests in mice to study postoperative delirium.High-throughput functional genomics identifies genes that ameliorate toxicity due to oxidative stress in neuronal HT-22 cells: GFPT2 protects cells against peroxideJNK2 translocates to the mitochondria and mediates cytochrome c release in PC12 cells in response to 6-hydroxydopamineThe antiapoptotic activity of melatonin in neurodegenerative diseases.Structure based molecular inhibition of Caspase-8 for treatment of multi-neurodegenerative diseases using known natural compounds.Multiple pathogenic proteins implicated in neuronopathic Gaucher disease miceThe metabolic enhancer piracetam ameliorates the impairment of mitochondrial function and neurite outgrowth induced by beta-amyloid peptideThe generation of a 17 kDa neurotoxic fragment: an alternative mechanism by which tau mediates beta-amyloid-induced neurodegeneration.Adiponectin is protective against oxidative stress induced cytotoxicity in amyloid-beta neurotoxicityInvolvement of oxidative stress in Alzheimer disease.Piracetam improves mitochondrial dysfunction following oxidative stress.Mitochondrial dysfunction - the beginning of the end in Alzheimer's disease? Separate and synergistic modes of tau and amyloid-β toxicityPhosphorylation of tau antagonizes apoptosis by stabilizing beta-catenin, a mechanism involved in Alzheimer's neurodegeneration.The carbonic anhydrase inhibitor methazolamide prevents amyloid beta-induced mitochondrial dysfunction and caspase activation protecting neuronal and glial cells in vitro and in the mouse brainMitochondrial dysfunction and Alzheimer's disease: role of amyloid-beta peptide alcohol dehydrogenase (ABAD).Nerve growth factor, neural stem cells and Alzheimer's disease.Signal transduction in Alzheimer disease: p21-activated kinase signaling requires C-terminal cleavage of APP at Asp664.Effects of Alzheimer's amyloid-beta and tau protein on mitochondrial function -- role of glucose metabolism and insulin signalling.Antioxidant activity of growth hormone-releasing hormone antagonists in LNCaP human prostate cancer line.Pharmacophore modeling and docking studies on some nonpeptide-based caspase-3 inhibitors.Effects of grape seed proanthocyanidin on Alzheimer's disease in vitro and in vivoHippocampal c-Jun-N-terminal kinases serve as negative regulators of associative learning.Molecular pathogenesis of Alzheimer's disease: reductionist versus expansionist approaches.The consequences of mitochondrial amyloid beta-peptide in Alzheimer's disease.Antioxidant protection: A promising therapeutic intervention in neurodegenerative disease.Pathological alteration in the choroid plexus of Alzheimer's disease: implication for new therapy approachesThe senescence hypothesis of disease progression in Alzheimer disease: an integrated matrix of disease pathways for FAD and SAD.Turning point in apoptosis/necrosis induced by hydrogen peroxide.Inducible antisense RNA targeting amino acid transporter ATB0/ASCT2 elicits apoptosis in human hepatoma cells.Implication of Caspase-3 as a Common Therapeutic Target for Multineurodegenerative Disorders and Its Inhibition Using Nonpeptidyl Natural CompoundsNucleofection of rat pheochromocytoma PC-12 cells with human mutated beta-amyloid precursor protein gene (APP-sw) leads to reduced viability, autophagy-like process, and increased expression and secretion of beta amyloid.Gene expression profiles of transcripts in amyloid precursor protein transgenic mice: up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimer's disease.Attenuation of oxidative damage-associated cognitive decline by Withania somnifera in rat model of streptozotocin-induced cognitive impairment.Expression of the hyperphosphorylated tau attenuates ER stress-induced apoptosis with upregulation of unfolded protein response.Evaluation of neuropathological effects of a high-fat high-sucrose diet in middle-aged male C57BL6/J mice.
P2860
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P2860
Neurotoxic mechanisms caused by the Alzheimer's disease-linked Swedish amyloid precursor protein mutation: oxidative stress, caspases, and the JNK pathway.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
2003年论文
@zh
2003年论文
@zh-cn
name
Neurotoxic mechanisms caused b ...... caspases, and the JNK pathway.
@en
type
label
Neurotoxic mechanisms caused b ...... caspases, and the JNK pathway.
@en
prefLabel
Neurotoxic mechanisms caused b ...... caspases, and the JNK pathway.
@en
P2093
P2860
P921
P356
P1476
Neurotoxic mechanisms caused b ...... caspases, and the JNK pathway.
@en
P2093
Astrid Bonert
Barbara Steiner
Celio A Marques
Walter E Muller
P2860
P304
28294-28302
P356
10.1074/JBC.M212265200
P407
P577
2003-05-01T00:00:00Z