Speakers: Dr Adam Walker, UQ and Dr Shuai Zhang, SUSTech
Host: Professor Helen Cooper & Professor Shengtao Hou
Date: Friday, September 10, 2021
Time: 12PM (noon) – 1PM Shenzhen // 2PM – 3PM Brisbane
Zoom: https://uqz.zoom.us/j/81168843400 


Meet the speakers

Dr Adam Walker

Senior Research Fellow and Group Leader, Queensland Brain Institute, The University of Queensland

Title: “Mechanisms of neurodegeneration and neuroprotection in amyotrophic lateral sclerosis and frontotemporal dementia”

Abstract: Accumulation of the primarily nuclear TAR DNA binding protein of 43 kDa (TDP-43) protein in the cytoplasm of neurons is characteristic of the neurodegenerative diseases amyotrophic lateral sclerosis/motor neuron disease (ALS/MND) and frontotemporal dementia (FTD). Both ALS and FTD lack effective treatments, however TDP-43 pathology is intimately linked with neurodegeneration. Pathological TDP-43 is aggregated, post-translationally modified and aberrantly interacts with numerous other proteins, which occurs concomitantly with loss of the normal functions of TDP-43. We have employed quantitative proteomics of cells and brain and spinal cord tissues of transgenic mouse models, as well as whole-genome CRISPR screening approaches, to define interactors and modulators of TDP-43 aggregation and toxicity. We are also developing adeno-associated viruses as tools for proof-of-concept studies in transgenic mice, and to create new mouse models of TDP-43 proteinopathies. These studies will improve our understanding of how neurons respond to TDP-43 pathology, and indicate potential modulators of TDP-43-mediated neurodegeneration. In the future, our findings could be harnessed as the basis for TDP-43-targeted disease-modulating therapeutics for ALS and FTD.


Dr Shuai Zhang

Research Assistant Professor, Professor Shengtao Hou’s Research Group, Southern University of Science and Technology

Title: “EphA4-Fc Reducing Brain Edema in Stroke”

Abstract: Activation of EphA4/Ephrin exacerbates disruption of the blood‑brain barrier (BBB) following cerebral ischemic/reperfusion (I/R) injury. So we aim to investigate the potential role and mechanism of EphA4-Fc, a patented inhibitor of EphA4 receptor, in I/R mouse model. The results indicated that EphA4-Fc administration before ischemia but not after reperfusion could markedly decrease brain injury. While EphA4-Fc administration before ischemia or after reperfusion reduced the brain edema. Therefore, EphA4-Fc was a potential drug for targeting post-stroke cerebral edema. Further evidences also showed that EphA4-Fc decreased BBB permeability and maintained the membrane levels of tight junction proteins after reperfusion for 24 h. Cytoskeletal proteins paly key roles in maintaining the membrane location of tight junction proteins in endothelial cell and AQP4 in astrocytes. So the further work will be focus on the mechanism of EphA4-Fc regulating the cytoskeletal proteins, which may be the reason of EphA4-Fc reducing the brain edema in stroke.   

About CNNE Seminar Series

The CNNE Seminar Series provides a forum for SUSTech and QBI members to showcase collaboration in key thematic areas and foster new projects.

All are welcome to join this meeting via ZOOM.