Michael Wong mainly investigates Epilepsy, Neuroscience, Epileptogenesis, Internal medicine and Tuberous sclerosis. While the research belongs to areas of Epilepsy, he spends his time largely on the problem of TSC1, intersecting his research to questions surrounding Astrocyte. His study looks at the relationship between Neuroscience and fields such as Kainic acid, as well as how they intersect with chemical problems.
His Epileptogenesis study combines topics from a wide range of disciplines, such as Neuroglia, Sirolimus, Status epilepticus and PI3K/AKT/mTOR pathway, Signal transduction. His research in Internal medicine intersects with topics in TOR Serine-Threonine Kinases, Endocrinology and Immunoelectrophoresis. His Tuberous sclerosis study integrates concerns from other disciplines, such as Cortical dysplasia and Cancer research.
Michael Wong mainly focuses on Epilepsy, Neuroscience, Epileptogenesis, Tuberous sclerosis and PI3K/AKT/mTOR pathway. His Epilepsy research is multidisciplinary, relying on both Kainic acid, Central nervous system disease, Disease, Pathology and TSC1. His work in Neuroscience tackles topics such as Neurotransmission which are related to areas like Excitatory postsynaptic potential and Neurotransmitter.
His Epileptogenesis study deals with Neuroglia intersecting with Potassium channel. His research on Tuberous sclerosis also deals with topics like
Michael Wong focuses on Tuberous sclerosis, Internal medicine, Neuroscience, TSC1 and PI3K/AKT/mTOR pathway. His work carried out in the field of Tuberous sclerosis brings together such families of science as Adverse effect, Randomized controlled trial, Everolimus, Dosing and Epilepsy. His biological study spans a wide range of topics, including Clinical endpoint, Drug resistance and Dose.
Michael Wong has researched Internal medicine in several fields, including Endocrinology and Oncology. Much of his study explores Neuroscience relationship to Neonatal brain. The various areas that Michael Wong examines in his PI3K/AKT/mTOR pathway study include Cortical dysplasia, Hemimegalencephaly, Epileptogenesis, Epilepsy in children and Penumbra.
His scientific interests lie mostly in Everolimus, Adverse effect, Dosing, Exosome and Nicotinamide phosphoribosyltransferase. The Everolimus study combines topics in areas such as Medical record, Discovery and development of mTOR inhibitors, Tuberous sclerosis and Sirolimus. His study on Adverse effect is covered under Internal medicine.
Michael Wong has included themes like Concomitant and Proportional hazards model in his Dosing study. His work in Exosome incorporates the disciplines of Extracellular, Hypothalamus, Extracellular vesicle, Cell biology and Adipose tissue. He integrates several fields in his works, including Nicotinamide phosphoribosyltransferase and Metabolism.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Rapamycin prevents epilepsy in a mouse model of tuberous sclerosis complex.
Ling-Hui Zeng;Lin Xu;David H. Gutmann;Michael Wong.
Annals of Neurology (2008)
The Mammalian Target of Rapamycin Signaling Pathway Mediates Epileptogenesis in a Model of Temporal Lobe Epilepsy
Ling-Hui Zeng;Nicholas R. Rensing;Michael Wong.
The Journal of Neuroscience (2009)
Astrocyte-specific TSC1 conditional knockout mice exhibit abnormal neuronal organization and seizures.
Erik J. Uhlmann;Michael Wong;Rebecca L. Baldwin;M. Livia Bajenaru.
Annals of Neurology (2002)
Mammalian target of rapamycin (mTOR) inhibition as a potential antiepileptogenic therapy: From tuberous sclerosis to common acquired epilepsies.
Michael Wong.
Epilepsia (2010)
The ketogenic diet inhibits the mammalian target of rapamycin (mTOR) pathway
Sharon S. McDaniel;Nicholas R. Rensing;Liu Lin Thio;Kelvin A. Yamada.
Epilepsia (2011)
Mechanisms of epileptogenesis in tuberous sclerosis complex and related malformations of cortical development with abnormal glioneuronal proliferation.
Michael Wong.
Epilepsia (2008)
Ketone bodies do not directly alter excitatory or inhibitory hippocampal synaptic transmission
Liu Lin Thio;Michael Wong;Kelvin A. Yamada.
Neurology (2000)
Tsc2 gene inactivation causes a more severe epilepsy phenotype than Tsc1 inactivation in a mouse model of Tuberous Sclerosis Complex
Ling-Hui Zeng;Nicholas R. Rensing;Bo Zhang;David H. Gutmann.
Human Molecular Genetics (2011)
Kainate Seizures Cause Acute Dendritic Injury and Actin Depolymerization In Vivo
Ling-Hui Zeng;Lin Xu;Nicholas R. Rensing;Philip M. Sinatra.
The Journal of Neuroscience (2007)
Prospective evaluation of treatment of Hemophilus influenzae meningitis
Ralph D. Feigin;Barbara W. Stechenberg;Margan J. Chang;Lisa M. Dunkle.
The Journal of Pediatrics (1976)
Epilepsy Currents
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