Project Title: Characterization of Glial & Neuronal Pathology Associated with Aβ Proteins in an Alzheimer’s Disease Model
Supervisor: Professor Paul Matthews
Location: 4th Floor, Burlington Danes, Hammersmith Campus
Having graduated with double BSc degrees in Biomedical Sciences from Queen Mary University of London (UK) and Clinical Medicine from Nanchang University (China), I was admitted by the Department of Brain Sciences at Imperial College London to join Prof. Paul Matthews’ laboratory, and Prof. Steve Gentleman is my secondary supervisor.
I am currently a student representative in Department of Brain Sciences, contributing on the organization of some social and party within the department, as well as reporting some common problems for students. I really enjoy the feeling of becoming an early-stage scientist, carrying out some interesting experiments that are hopefully the milestones of dementia research. In my spare time, I love writing novels and playing tennis, ping pong, badminton and bowling.
2018 Aug - present
PhD in Clinical Medicine Research, Imperial College London, UK
2013 Sep - 2018 Jun
BSc in Biomedical Sciences, Queen Mary University of London, UK
BSc in Clinical Medicine, Nanchang University, China
Alzheimer’s Disease (AD) is the most common type of late-life dementia. Glial activation, Aβ deposition, neuronal death and synaptic loss are four hallmarks of AD. Cellular homeostasis in the CNS is regulated and maintained in part by microglia and astrocytes. Activated microglia undergo polarization and become pro-inflammatory or anti-inflammatory. Astrocytes are important regulators of CNS homeostasis, metabolism and synaptic transmission, functionally integrated with microglia, and likely play central pathological roles in chronic neurodegeneration disease as AD. However, although Aβ deposits are surrounded by activated microglia and astrocytes in AD, it remains uncertain whether this is a consequence of the Aβ plaques or whether they contribute to their genesis. The relation of these two pathological elements to neurodegeneration also remains surprisingly unclear. My research interest is focused on early stage AD, and my project is based on the AppNL-G-F mouse, a triple knock-in mouse model which avoids the artefact caused by transfecting too many APP gene copies.
Huang D, Wang Y, Tang J, et al. Molecular mechanisms of suppressor of fused in regulating the hedgehog signalling pathway. Oncology letters, 2018. 15(5): p. 6077-6086.
Presentations and Conferences
2018 - 2020 UK Dementia Research Institute Connectome
2019 - 2020 Meeting of British Neuropathological Society
2019 Invited Talk in School of Biological and Chemical Sciences, Queen Mary University of London