A role for vascular deficiency in retinal pathology in a mouse model of ataxia-telangiectasia

Keyphrases

• Mouse Model 100%
• Ataxia Telangiectasia 100%
• Gene-deficient Mice 100%
• Retinal Pathology 100%
• Mouse Retina 50%
• Central Nervous System 33%
• Aged Mice 33%
• Occludin 33%
• Etiology 16%
• Morphological Changes 16%
• Metabolic Activity 16%
• Aberrations 16%
• Vascularization 16%
• Protein Kinase 16%
• Disease Stage 16%
• Immunohistochemistry 16%
• Neurodegeneration 16%
• DNA Damage 16%
• Vascular Endothelial Growth Factor 16%
• ATM Gene 16%
• Null mutation 16%
• Fibrinogen 16%
• Angiography 16%
• Retina 16%
• Cell Interaction 16%
• Advanced Stage 16%
• Functional Deficits 16%
• Glial Cells 16%
• Fainting 16%
• DNA Damage Response 16%
• Tight Junction Proteins 16%
• Glial Fibrillary Acidic Protein 16%
• Retinal Tissue 16%
• Retinal Neurons 16%
• Vascular Leakage 16%
• Retinal Vasculature 16%
• Vascular Abnormalities 16%

Neuroscience

• Ataxia Telangiectasia 100%
• Central Nervous System 66%
• Occludin 66%
• Messenger RNA 66%
• DNA Damage 33%
• Microglia 33%
• DNA Damage Response 33%
• Vascular Endothelial Growth Factor 33%
• Immunohistochemistry 33%
• Neurodegeneration 33%
• ATM Protein 33%
• Fibrinogen 33%
• Cell Interaction 33%
• Tight Junction Protein 33%
• Glial Fibrillary Acidic Protein 33%
• Retinal Neuron 33%
• Angiography 33%