Date: 2 May 2024 (Thursday)
Time: 5:00 pm – 6:00 pm
Venue: Seminar Room 4, G/F, Laboratory Block, 21 Sassoon Road 

5:00 p.m.

Presenter: Yik Chai Charles LAU (PhD candidate)
Primary Supervisor: Prof. Jason WONG
Presentation Title: Whole-genome bisulphite investigation into mechanisms underlying ageing and epigenetic clock function
Abstract: Epigenetic clocks are models used to predict age and related phenomena including mortality, frailty, and risk of developing ageing-associated disorders, and have emerged as among the most robust and accurate biomarkers for age. Despite their utility, the nature and function of CpGs that constitute such clocks remain poorly-characterized. Elucidating the epigenetics that underlie clock CpGs thus is a promising route to understanding ageing comprehensively. With the use of solely WGBS datasets to identify novel CpGs and to remove biases inherent to DNA methylation arrays, we found and analysed general features underlying established and custom-made clocks and their associated clock and clock-like CpGs through enrichment analyses in respect to genomic, chromatin and proteomic features, and validated and tested clock algorithms. Results include the consistent enrichment of quiescent state and the subset-dependent enrichment of enhancer and promoter-associated CpGs. Further work will focus on finding the molecular function of clock and clock-like CpGs.

5:30 p.m.

Presenter: Peiyi XIAO (PhD candidate)
Primary Supervisor: Prof. Raymond CHANG
Presentation Title:  Investigating the role of free radicals and inflammation on the spread of pathological factors in Parkinson’s Disease
Abstract:  Loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and Lewy bodies in neurons are two major pathological hallmarks of the Parkinson’s disease (PD). The spread of a-synuclein to other brain regions may explain deficits of brain functions other than motor problems. However, it is still a major question in PD research field. While free radicals and inflammation play an important role in the pathogenesis of PD, it is unclear whether these two factors also make impact in the spreading of α-synuclein to other brain regions. This study aims to investigate whether free radicals and systemic inflammation affect the spread of pathological factors in experimental models of PD. In 6-hydroxydopamine (6-OHDA) mice model, we found intense oxidative stress in the ipsilateral hippocampus. However, there was no significant change in cognitive impairment, neuronal loss, and phosphorylation of a-synuclein/tau proteins in the ipsilateral hippocampus. We are now evaluating the effects of oxidative stress and systemic inflammation in another experimental PD model by intracerebral injection of adeno-associated virus expressing human a-synuclein (AAV-α-synuclein). It is anticipated that we can delineate the factors affecting the motor deficits and other brain functions in the pathogenesis of PD.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Jerry Siu at 3917 6912.