Hippocampal RAGE immunoreactivity in early and advanced Alzheimer's disease - Wikidata - awgldk - TriplyDB

Hippocampal RAGE immunoreactivity in early and advanced Alzheimer's disease

Hippocampal RAGE immunoreactivity in early and advanced Alzheimer's disease

http://www.wikidata.org/entity/Q36977898

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Receptor for advanced glycation end products and its involvement in inflammatory diseases The Possible Role of Antioxidant Vitamin C in Alzheimer's Disease Treatment and Prevention The multiple faces of RAGE--opportunities for therapeutic intervention in aging and chronic disease Alteration of Aβ metabolism-related molecules in predementia induced by AlCl3 and D-galactose Receptor for advanced glycation end products is upregulated in optic neuropathy of Alzheimer's disease.Receptor for advanced glycation endproduct modulators: a new therapeutic target in Alzheimer's disease.Impaired lipoprotein receptor-mediated peripheral binding of plasma amyloid-β is an early biomarker for mild cognitive impairment preceding Alzheimer's disease Association of the RAGE G82S polymorphism with Alzheimer's disease.Low-density lipoprotein receptor-related protein-1: a serial clearance homeostatic mechanism controlling Alzheimer's amyloid β-peptide elimination from the brain Clearance of amyloid-beta peptide across the blood-brain barrier: implication for therapies in Alzheimer's disease.Human apolipoprotein E ɛ4 expression impairs cerebral vascularization and blood-brain barrier function in mice Amyloid-beta transporter expression at the blood-CSF barrier is age-dependent.Neurovascular defects and faulty amyloid-β vascular clearance in Alzheimer's disease Consequences of Aberrant Insulin Regulation in the Brain: Can Treating Diabetes be Effective for Alzheimer's Disease.Glio-vascular changes during ageing in wild-type and Alzheimer's disease-like APP/PS1 mice.Low-density lipoprotein receptor-related protein 1: a physiological Aβ homeostatic mechanism with multiple therapeutic opportunities.Neurovascular dysfunction and faulty amyloid β-peptide clearance in Alzheimer disease.Glycation exacerbates the neuronal toxicity of β-amyloid.Blood-brain barrier dysfunction as a cause and consequence of Alzheimer's disease.Receptor for advanced glycation end products: its role in Alzheimer's disease and other neurological diseases.Trientine reduces BACE1 activity and mitigates amyloidosis via the AGE/RAGE/NF-κB pathway in a transgenic mouse model of Alzheimer's disease.Increased expression of the receptor for advanced glycation end products in neurons and astrocytes in a triple transgenic mouse model of Alzheimer's disease.Crosstalk between calcium, amyloid beta and the receptor for advanced glycation endproducts in Alzheimer's disease.Amyloid-modifying therapies for Alzheimer's disease: therapeutic progress and its implications.The distributional nexus of choroid plexus to cerebrospinal fluid, ependyma and brain: toxicologic/pathologic phenomena, periventricular destabilization, and lesion spread.Systemic and central immunity in Alzheimer's disease: therapeutic implications.Is RAGE still a therapeutic target for Alzheimer's disease?Neurodegeneration, β-amyloid and mood disorders: state of the art and future perspectives.The role of vitamin D in Alzheimer's disease: possible genetic and cell signaling mechanisms.RAGE regulation and signaling in inflammation and beyond.Drug access to the central nervous system in Alzheimer's disease: preclinical and clinical insights.Age-Dependent Regulation of the Blood-Brain Barrier Influx/Efflux Equilibrium of Amyloid-β Peptide in a Mouse Model of Alzheimer's Disease (3xTg-AD).In vitro and in vivo characterization of several functionalized ultrasmall particles of iron oxide, vectorized against amyloid plaques and potentially able to cross the blood-brain barrier: toward earlier diagnosis of Alzheimer's disease by molecula Can insulin signaling pathways be targeted to transport Aβ out of the brain?Vitamin C, Aging and Alzheimer's Disease.Targeting the Receptor for Advanced Glycation Endproducts (RAGE): A Medicinal Chemistry Perspective.Potentiating role of copper on spatial memory deficit induced by beta amyloid and evaluation of mitochondrial function markers in the hippocampus of rats.Common neurodegenerative pathways in obesity, diabetes, and Alzheimer's disease.A Novel, Multi-Target Natural Drug Candidate, Matrine, Improves Cognitive Deficits in Alzheimer's Disease Transgenic Mice by Inhibiting Aβ Aggregation and Blocking the RAGE/Aβ Axis.Sex Hormone Decline and Amyloid β Synthesis, Transport and Clearance in the Brain.

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P2860

Hippocampal RAGE immunoreactivity in early and advanced Alzheimer's disease

http://www.wikidata.org/entity/Q36977898

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

@zh-tw

2008年论文

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2008年论文

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2008年论文

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name

Hippocampal RAGE immunoreactivity in early and advanced Alzheimer's disease

@en

type

label

Hippocampal RAGE immunoreactivity in early and advanced Alzheimer's disease

@en

prefLabel

Hippocampal RAGE immunoreactivity in early and advanced Alzheimer's disease

@en

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J.BRAINRES.2008.06.124

P1433

P1476

Hippocampal RAGE immunoreactivity in early and advanced Alzheimer's disease

@en

P2093

Edward G Stopa

http://www.w3.org/2001/XMLSchema#string

Gerald D Silverberg

http://www.w3.org/2001/XMLSchema#string

John E Donahue

http://www.w3.org/2001/XMLSchema#string

Liliana Gonzalez

http://www.w3.org/2001/XMLSchema#string

Miles C Miller

http://www.w3.org/2001/XMLSchema#string

Rosemarie Tavares

http://www.w3.org/2001/XMLSchema#string

Virginia Hovanesian

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P2860

Role of the Blood-Brain Barrier in the Pathogenesis of Alzheimers Disease

RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease

S100B and S100A6 differentially modulate cell survival by interacting with distinct RAGE (receptor for advanced glycation end products) immunoglobulin domains

Neuropathological stageing of Alzheimer-related changes

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide

The Consortium to Establish a Registry for Alzheimer's Disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer's disease

The blood-brain barrier in health and chronic neurodegenerative disorders

Clearance of Alzheimer's amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier

Neuronal origin of a cerebral amyloid: neurofibrillary tangles of Alzheimer's disease contain the same protein as the amyloid of plaque cores and blood vessels.

Toward a comprehensive theory for Alzheimer's disease. Hypothesis: Alzheimer's disease is caused by the cerebral accumulation and cytotoxicity of amyloid beta-protein.

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273-280

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scholarly article

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10.1016/J.BRAINRES.2008.06.124

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P478

1230

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Conrad Johanson

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2008-07-14T00:00:00Z

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P5875

51430591

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18657529

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Alzheimer's disease

P932

2585053

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