A5000620021- Neuroscience and Neuropharmacology Research
- Neural dynamics and brain function
- Tryptophan and brain disorders
- CRISPR and Genetic Engineering
- Neurogenesis and neuroplasticity mechanisms
- Alzheimer's disease research and treatments
- Pluripotent Stem Cells Research
- 3D Printing in Biomedical Research
- Genetics and Neurodevelopmental Disorders
- Photoreceptor and optogenetics research
Stanford University
2019-2023
Massachusetts Institute of Technology
2020
Presenilin mutations that alter γ-secretase activity cause familial Alzheimer's disease (AD), whereas ApoE4, an apolipoprotein for cholesterol transport, predisposes to sporadic AD. Both and AD feature synaptic dysfunction. Whether is involved in metabolism whether such involvement impacts function remains unknown. Here, we show human neurons, chronic pharmacological or genetic suppression of increases synapse numbers but decreases transmission by lowering the presynaptic release probability...
Many neurodevelopmental disorders are characterized by impaired functional synaptic plasticity and abnormal dendritic spine morphology, but little is known about how these related. Previous work in the Fmr1-/y mouse model of fragile X (FX) suggests that increased constitutive protein synthesis yields exaggerated mGluR5-dependent long-term depression (LTD) area CA1 hippocampus, an effect on structural remains to be determined. In current study, we used simultaneous electrophysiology...
At tripartite synapses, astrocytes enmesh synaptic contacts, but how contribute to the formation, maturation and plasticity of synapses remains elusive. Here we show that both neurons abundantly express neurexin-1, a presynaptic adhesion molecule controls properties. Using super-resolution imaging, demonstrate neuronal astrocytic neurexin-1 form discrete nanoclusters at excitatory synapses. We find distinct patterns heparan sulfate modification alternative splicing confer onto different...