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Cao Mian

Assistant Professor

Principal Investigator

Laboratory of Cellular Neuroscience & Neurodegeneration

Email

Contact: 65161096

Dr Cao is an Assistant Professor in the Neuroscience and Behavioural Disorders programme at Duke-NUS Medical School. His research focuses on the functional relationship of several Parkinson’s disease genes with the endocytic traffic of synaptic vesicles. He earned his PhD in Biochemistry from the Hong Kong University of Science and Technology in 2009, and subsequently joined Dr Pietro De Camilli’s laboratory at Yale University/Howard Hughes Medical Institute as a Postdoctoral Associate in the Department of Cell Biology. He was then promoted to Associate Research Scientist in the Department of Neuroscience at Yale University in 2015.

Dr Cao’s work has been published in several high impact journals, such as Neuron, PLoS Biology and The Journal of Neuroscience. Several prestigious foundations working on Parkinson’s disease have supported his research, including postdoctoral fellowships from the American Parkinson’s Disease Association, the Parkinson’s Disease Foundation, and the Michael J. Fox Foundation for Parkinson’s Research.

Parkinson's disease (PD) is the second most common neurodegenerative disorder. Genetic studies have recently identified several PD-linked proteins that are involved in endocytic trafficking at the synapse, suggesting impaired synaptic transmission is an early feature of PD. The long-term goal of my laboratory is to elucidate the pathogenic mechanisms of PD and reveal new potential therapeutic targets for the treatment of PD. Specifically, we will investigate how the impaired synaptic membrane trafficking results in selective neurodegeneration of dopaminergic neurons in PD. We will also study the potential synergistic function of several PD-linked proteins on synaptic endocytic pathway. Previously, we have identified a novel PD mutation in Synaptojanin1/PARK20, and developed a Knock-In mouse model which recapitulates human patients’ manifestations. We plan to perform biochemical, cell biological, genetic, physiological, pathological and behavioral experiments to address these questions using the PD mouse models and iPSC-derived human patient neurons.

Visit https://caomianlabdukenus.wordpress.com/ for more information.

  1. Jin W, Ge WP, Xu J, Cao M, Peng L, Yung W, Liao D, Duan S, Zhang M, Xia J. Lipid binding regulates synaptic targeting of PICK1, AMPA receptor trafficking, and synaptic plasticity. J Neurosci. 2006 Mar 1; 26(9): 2380-90.
  2. Cao M, Xu J, Shen C, Kam C, Huganir RL, Xia J. PICK1-ICA69 Heteromeric BAR Domain Complex Regulates Synaptic Targeting and Surface Expression of AMPA Receptors. J Neurosci. 2007 Nov 21; 27(47): 12945-56.
  3. Cao M*, Mao Z*, Kam C, Xiao N, Cao XX, Shen C, Cheng KY, Xu AM, Lee KM, Jiang LW, Xia J. PICK1 and ICA69 Control Insulin Granule Trafficking and Their Deficiencies Lead to Impaired Glucose Tolerance. * These authors contributed equally to this work. PLOS Biology 2013;11(4):e1001541.
  4. Krebs CE, Karkheiran S, Powell JC, Cao M, Makarov V, Darvish H, Di Paolo G, Walker RH, Shahidi GA, Buxbaum JD, De Camilli P, Yue Z, Paisán-Ruiz C. The Sac1 domain of SYNJ1 identified mutated in a family with early-onset progressive parkinsonism with generalized seizures. Hum Mutat. 2013 Sep;34(9):1200-7.
  5. Cao M, Milosevic I, Giovedi S, De Camilli P. Up-regulation of Parkin in endophilin mutant mice. J Neurosci. 2014 Dec 3; 34(49): 16544-9.
  6. Hardies K, Cai Y, Jardel C, Jansen AC, Cao M, May P, Djémié T, Hachon Le Camus C, Keymolen K, Deconinck T, Bhambhani V, Long C, Sajan SA, Helbig KL; AR working group of the EuroEPINOMICS RES Consortium., Suls A, Balling R, Helbig I, De Jonghe P, Depienne C, De Camilli P, Weckhuysen S. Loss of SYNJ1 dual phosphatase activity leads to early onset refractory seizures and progressive neurological decline. Brain. 2016 Sep; 139(Pt 9):2420-30.
  7. Cao M, Wu YM, McCartney A, Ashrafi G, Wheeler H, Bushong EA, Boassa D, Ellisman MH, Ryan TA and De Camilli P. Parkinsonism mutation in Synaptojanin 1 leads to impaired synaptic vesicle recycling and synaptic degeneration in dopaminergic neurons. Neuron 2017 Feb 22;93(4):882-896. (F1000 Prime recommended)