Gad67 haploinsufficiency reduces amyloid pathology and rescues olfactory memory deficits in a mouse model of Alzheimer's disease

Keyphrases

• Memory Deficits 100%
• Amyloid Pathology 100%
• Haploinsufficiency 100%
• Alzheimer's Disease Model 100%
• Glutamic Acid Decarboxylase 65 (GAD65) 100%
• GAD67 100%
• Alzheimer's Disease Pathology 37%
• Alzheimer's Disease 25%
• Green Fluorescent Protein 25%
• Epilepsy 12%
• Functional Role 12%
• Between-group 12%
• Glutamate 12%
• Neurotransmitter Systems 12%
• Immunostaining 12%
• Mouse Brain 12%
• Schizophrenia 12%
• Neurological Disorders 12%
• Alzheimer's Disease Brain 12%
• Cognitive Deficits 12%
• Electrophysiological Examination 12%
• Behavioral Tests 12%
• Astrocytic 12%
• Putative Drug Targets 12%
• Disease-causing mutations 12%
• Green Fluorescent Protein Gene 12%
• Haploinsufficient 12%
• ELISA Test 12%
• Age-related Neurodegeneration 12%
• Glutamatergic System 12%
• GABAergic System 12%
• Familial Alzheimer's Disease 12%

Neuroscience

• Alzheimer's Disease 100%
• Amnesia 100%
• Amyloid Protein 100%
• Haploinsufficiency 100%
• Glutamate Decarboxylase 67 80%
• Gamma-Aminobutyric Acid 40%
• Green Fluorescent Protein 30%
• Behavior (Neuroscience) 10%
• Cognitive Disorders 10%
• Glutamic Acid 10%
• Neurotransmitter 10%
• Nervous System Disorder 10%
• Cholinergic 10%
• ELISA 10%
• Immunohistochemistry 10%
• Dipeptidyl Carboxypeptidase 10%
• Familial Alzheimer's Disease 10%
• Mouse Brain 10%