A circuitry and biochemical basis for tuberous sclerosis symptoms: From epilepsy to neurocognitive deficits

Keyphrases

• Aberrations 16%
• Autosomal Dominant 16%
• Benign Tumor 16%
• Biological Basis 100%
• Brain Lesions 33%
• Brain Malformation 16%
• Cell Substrate 16%
• Cellular Mechanisms 16%
• Circuitry 100%
• Cognitive Defects 16%
• Cognitive Difficulties 16%
• Cognitive Impairment 16%
• Complex Patients 16%
• Complex Research 16%
• Cortical Lesions 33%
• Electroporation 16%
• Epilepsy 100%
• Epileptogenesis 16%
• Hydrocephalus 16%
• Hyperactivity 16%
• Inactivating mutation 16%
• Increased Activity 16%
• Loss of Heterozygosity 33%
• Mammalian Target of Rapamycin (mTOR) 50%
• Molecular Mechanism 16%
• Monogenetic 16%
• Mouse Model 16%
• Mutant Alleles 16%
• Neurocognitive Deficits 100%
• Neurological Manifestations 16%
• Neurological Presentations 16%
• Neuronal Circuit Formation 16%
• Neuronal Defects 16%
• Neuronal Function 33%
• Neuropsychiatric Problems 16%
• Novel Therapeutic Targets 16%
• Perinatal Development 16%
• Potential Consequences 16%
• Psychological Impairment 16%
• Seizure 16%
• Synaptic Plasticity 16%
• TSC1 16%
• Tuberous Sclerosis 100%
• Tuberous Sclerosis Complex 100%

Neuroscience

• Brain Lesion 33%
• Cognitive Disorders 16%
• Electroporation 16%
• Epileptogenesis 16%
• Hydrocephalus 16%
• Hyperactivity 16%
• Mammalian Target of Rapamycin 50%
• Synaptic Plasticity 16%
• TSC1 16%
• Tuberous Sclerosis 100%