Activation of Wnt/β-catenin pathway mitigates blood-brain barrier dysfunction in Alzheimer's disease

Keyphrases

• Catenin 100%
• Alzheimer's Disease 100%
• Blood-brain Barrier Disruption 100%
• Blood-brain Barrier 71%
• Brain Endothelial Cells 42%
• Glucose Transporter 1 (GLUT1) 28%
• LRP6 28%
• APPswe 28%
• APPswePS1dE9 28%
• Hippocampus 14%
• Barrier Function 14%
• Treatment Strategy 14%
• Age-dependent 14%
• Cortex 14%
• Pathophysiology 14%
• Fibrinogen 14%
• Cognitive Decline 14%
• Neurodegenerative Diseases 14%
• Potential Treatments 14%
• Wnt Signaling 14%
• Disease Mechanisms 14%
• Alzheimer's Disease Model 14%
• Major Contributor 14%
• Glycogen Synthase Kinase 3 (GSK3) 14%
• AKT Pathway 14%
• Upstream Regulator 14%
• Disease Stage 14%
• Tight Junction Proteins 14%
• Optogenetic Tools 14%
• Neurological Deterioration 14%
• Cerebral Microcirculation 14%
• Brain Endothelium 14%
• Claudin-5 14%
• Barrier Repair 14%
• Planar Cell Polarity Pathway 14%

Neuroscience

• Catenin 100%
• Alzheimer's Disease 100%
• Blood Brain Barrier 100%
• Amyloid Protein 37%
• Low Density Lipoprotein Receptor Related Protein 6 25%
• Hippocampus 12%
• Fibrinogen 12%
• Microvessel 12%
• Neurodegenerative Disorder 12%
• Optogenetics 12%
• Wnt Signaling Pathway 12%
• Protein Kinase B 12%
• Glucose Transporter 12%
• Claudin 5 12%
• Tight Junction Protein 12%
• Cell Polarity 12%

Pharmacology, Toxicology and Pharmaceutical Science

• Alzheimer's Disease 100%
• Catenin 100%
• Blood-Brain Barrier 100%
• Amyloid Protein 37%
• Diseases 37%
• Mouse Model 12%
• Fibrinogen 12%
• Pathophysiology 12%
• Glucose Transporter 12%
• Protein Kinase B 12%
• Tight Junction Protein 12%
• Claudin 5 12%