Research Departments & Organizations
The brain is a wonderful and mysterious machine, which makes us who we are. The activity of billions of neurons and glia orchestrate our thoughts and daily life. However, alterations in the number of neurons, their misplacement, or changes in the way they receive, handle, or send information can negatively impact our brain function and our lives. A mutation in a single gene can lead to such alterations resulting in a specific pathology and disorder. Our Mission is to understand how a mutated, dysfunctional protein will lead to abnormal brain formation and function.
Specialized Terms: Neurogenesis; stem cells; mTOR; Neural stem cell; Cognitive functions; autism
Extensive Research Description
Our attention has been focused on the mammalian Target of Rapamycin, mTOR. mTOR is a converging point in cell signaling, or in other terms an intracellular hub, that receives signals from diverse intracellular routes and extracellular ligands. Importantly, mTOR is dysregulated in many neurological disorders. These disorders referred to as mTORopathies include (but are not limited to) Tuberous Sclerosis Complex (TSC), autism, Alzheimer's disease, and Schizophrenia. We have focused on TSC, to better understand the circuit basis of mental retardation and autism.
Our work has the following three lines of research related to the following keywords: mTOR- Neural stem cell- Neurogenesis-Cognitive functions- mTORopathies
1. Understanding how a circuit is formed from neural stem cells to synaptic integration in health and in developmental mTORopathies.
2. Preventing lesion formations and associated neurological symptoms in TSC and other developmental mTORopathies.
3. Understanding the molecular basis of cognitive dysfunctions in TSC.
Neurobiology France (2008)
Professor Bordey conducts collaborative research with French neurobiologists
Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice.
Feliciano DM, Su T, Lopez J, Platel JC, Bordey A. Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice. The Journal Of Clinical Investigation 2011, 121:1596-607. 2011
NMDA receptors activated by subventricular zone astrocytic glutamate are critical for neuroblast survival prior to entering a synaptic network.
Platel JC, Dave KA, Gordon V, Lacar B, Rubio ME, Bordey A. NMDA receptors activated by subventricular zone astrocytic glutamate are critical for neuroblast survival prior to entering a synaptic network. Neuron 2010, 65:859-72. 2010
GABA's control of stem and cancer cell proliferation in adult neural and peripheral niches.
Young SZ, Bordey A. GABA's control of stem and cancer cell proliferation in adult neural and peripheral niches. Physiology (Bethesda, Md.) 2009, 24:171-85. 2009
The astrocyte odyssey.
Wang DD, Bordey A. The astrocyte odyssey. Progress In Neurobiology 2008, 86:342-67. 2008
Nonsynaptic GABA signaling in postnatal subventricular zone controls proliferation of GFAP-expressing progenitors.
Liu X, Wang Q, Haydar TF, Bordey A. Nonsynaptic GABA signaling in postnatal subventricular zone controls proliferation of GFAP-expressing progenitors. Nature Neuroscience 2005, 8:1179-87. 2005