- Title Instructor, Harris Laboratory
- Education PhD: Penn State University
Postdoctoral training: Oregon Health and Science University
- Office K2
- Email firstname.lastname@example.org
- Phone 617-638-4117
- Area of Interest Neuroscience, neurodegenerative diseases, dendritic spine, primary neurons, prion diseases, alzheimer’s diseases
Prion disease represents a group of diseases that affect both humans and animals. In humans with prion diseases, the brain functions will be impaired, causing changes in memory, personality and behavior.
The causes of prion diseases can be sporadic, inherited due to a faulty gene, or infected. The infected form of prion diseases is the only infectious disease that doesn’t involve DNA nor RNA but only protein. Because it’s an infectious disease, much of the effort in the field has been focusing on preventing its infectivity. However, prion disease is also a devastating neurodegenerative disease with no cure. Little is known about the mechanisms of prion disease, which is mostly due to the lack of in vitro assay to report its neuronal toxicity.
The goal of my research is to set up an in vitro model to study scrapie’s neuronal toxicity using primary mouse neurons. There is literature suggesting that synapse loss is an early sign in mice infected with scrapie, the infectious version of PrPc. So I will focus on its synaptotoxicity first. In the long term, I would like to use this system to understand a few fundamental questions in the prion field : 1) What’s the downstream molecular mechanisms of scrapie’s synatotoxicity 2) Despite prion diseases and Alzheimer’s diseases all induce synaptotoxicity, how similar are the molecular pathways 3) Is infectivity associated with toxicity in Prion diseases.
Fang C, Imberdis T, Garza MC, Wille H, Harris DA. A Neuronal Culture System to Detect Prion Synaptotoxicity. PLoS Pathog. 2016 May; 12(5):e1005623. PMID: 27227882.
Fang C, Decker H, Banker G. Axonal transport plays a crucial role in mediating the axon-protective effects of NmNAT. Neurobiol Dis. 2014 Aug; 68:78-90. PMID: 24787896.
Fang C, Bourdette D, Banker G. Oxidative stress inhibits axonal transport: implications for neurodegenerative diseases. Mol Neurodegener. 2012; 7:29. PMID: 22709375.
Winter MR, Fang C, Banker G, Roysam B, Cohen AR. Axonal transport analysis using Multitemporal Association Tracking. Int J Comput Biol Drug Des. 2012; 5(1):35-48. PMID: 22436297.
Deng L, Yao J, Fang C, Dong N, Luscher B, Chen G. Sequential postsynaptic maturation governs the temporal order of GABAergic and glutamatergic synaptogenesis in rat embryonic cultures. J Neurosci. 2007 Oct 3; 27(40):10860-9. PMID: 17913919.
Fang C, Deng L, Keller CA, Fukata M, Fukata Y, Chen G, Lüscher B. GODZ-mediated palmitoylation of GABA(A) receptors is required for normal assembly and function of GABAergic inhibitory synapses. J Neurosci. 2006 Dec 6; 26(49):12758-68. PMID: 17151279.
Complete list can be found at BU Profiles