Han-Jou Chen

Accepting PhD Students

PhD projects

1) Cell-specific response to TDP-43 in ALS
TDP-43 is the main component of the hallmark pathology linked to the motor neurone disease, ALS. Studies show that the overexpression or disruption of TDP-43 promotes the aggregations in affected cells, and drives disease development and progression. Despite motor neurones are the primary cells affected in ALS, ours and other recent studies have suggested that other CNS cells are also affected by TDP-43 expression, albeit to a different extent.
To further dissect the molecular pathgenesis of TDP-43-mediated neurodegeneration, we are recruiting students to embark on new research investigating
- how different CNS cells respond to TDP-43 disruption
- how different interact with each other during neurodegeneration
The project will use multiple models including CRISPR-edited cells, established cell lines, rodent primary cells, human iPSCs and transgenic animals, and employ a wide range of research techniques including bioinformatics analysis for transcriptomic study, molecular/cellular analysis and animal behaviour assays.

2) Searching for novel chaperone activator for neurodegenerative disease treatment.
The accumulation of protein aggregates is the common pathology for nearly all neurodegenerative diseases. These aggregates cause toxicity to the neurones and are the primary targets for therapeutic development for neurodegenerative diseases. In our and others' previous studies, it has been established that the upregulation of chaperone response can effectively resolve protein aggregates and rescue phenotypic disruption. To explore the potential in drug development targeting chaperone response in neurodegenerative disease treatment, this project aims to
- characterise the regulatory machinery for the master controller of the chaperone response, HSF1
- building an in vitro reporter assay for drug screening
This project will use in vitro models to study structural biology, protein-protein interactions and chaperone response. We will work with biophysicists to characterise the regulation of HSF1 and utilise the findings to construct a reporter assay suitable for high throughput drug screening.