• Title Instructor, Harris laboratory
  • Education PhD: Institute of Neuroscience, Chinese Academy of Sciences
    Postdoctoral training: Brigham and Women’s Hospital
  • Office K2
  • Phone 617-638-4117
  • Area of Interest neurobiology, electrophysiology, neurodegenerative diseases, Alzheimer’s disease, prion disease

Prion diseases, or transmissible spongiform encephalopathies, comprise a group of rapidly progressive and invariably fatal neurodegenerative disorders for which there are no effective treatments or cures. Much is known about prion infection and propagation, which is mediated by the conversion of the cellular prion protein (PrPC) to an aggregated isoform (PrPSc) through a self-templating mechanism. However, the pathways underlying prion-mediated neurotoxicity are poorly understood, and progress has been hampered by the lack of robust cellular assays. Deletion of conserved residues in the central region of PrP has been shown to produce a highly toxic molecule (ΔCR PrP) that causes death within a week of birth in mice lacking wild-type PrP. Deletion of conserved residues in the central region of PrP has been shown to produce a highly toxic molecule (ΔCR PrP) that causes death within a week of birth in mice lacking wild-type PrP. ΔCR PrP induces large, spontaneous inward currents.

My research work is focused on: 1) to understand the mechanism of PrP-induced abnormal ionic activities using electrophysiological method 2) to investigate how the mutated forms of PrP or anti-prion antibodies, which induce spontaneous currents, induce neuronal toxicity 3) to investigate whether PrP-induced currents are the pathogenic mechanism underlying prion toxicity.

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