School of Biomedical Sciences is pleased to invite you to join the following seminar:

Date: 22 Aug 2023 (Tue)
Time: 4:00 pm – 5:00 pm
Venue: Lecture Theatre 1, 1/F, 3 Sassoon Road

Speaker: Dr Evandro Fei Fang, Associate Professor, University of Oslo and Akershus University Hospital, Norway
Talk Title: The '4A's: Ageing, Alzheimer's disease, autophagy, and artificial intelligence

Co-organizers: School of Biomedical Sciences, HKUMed; Hong Kong Society of Cell Biology
 

Biography
Evandro F. Fang is an Associate Professor of Molecular Gerontology at the University of Oslo (UiO) and the Akershus University Hospital, Norway, and his group are working on the molecular mechanisms of human ageing and age-predisposed neurodegeneration (https://evandrofanglab.com/). More specifically, the Fang laboratory is focusing on the molecular mechanisms behind how cells clear their damaged and aged mitochondria, a process termed “mitophagy”, as well as the roles of the NAD⁺-mitophagy/autophagy axis in healthy ageing and AD inhibition. NAD⁺ is a fundamental molecule in life and health and decreases in ageing and AD. Dr Fang is fascinated with and actively engaged in moving his laboratory findings to translational applications and is involved in 5 NAD⁺-based clinical trials, with the overarching goal of establishing novel and safe biological approaches to promote longer and healthier human lives.

Abstract
Increased lifespan enables people to live longer, but not necessarily healthier lives. Ageing is arguably the highest risk factor for numerous human diseases, including Alzheimer’s disease (AD); thus understanding the molecular mechanisms of human aging holds the promise of developing interventional and therapeutic strategies for many diseases simultaneously, promoting healthy longevity. Accumulation of damaged mitochondria is a hallmark of aging and age-related AD. However, the molecular mechanisms of impaired mitochondrial homeostasis and their relationship to AD are still elusive. Mitochondrial autophagy (mitophagy) is the cellular self-clearing process that removes damaged and superfluous mitochondria, and therefore plays a fundamental role in maintaining neuronal homeostasis and survival. We hypothesise that age-susceptible defective mitophagy causes accumulation of damaged mitochondria, which in combination with the two AD-defining pathologies, Aβ plaques and tau tangles, further exacerbates AD onset and progression. Restoration of mitophagy, through pharmaceutical (e.g., NAD⁺, passion fruit components, and urolithin A) and genetic approaches, forestalls pathology and cognitive decline in mouse models of AD and improves neuronal function in AD iPSC-derived neurons. Additionally, artificial intelligence (AI) is now being used to propel drug screening, as well as being used for drug design specifically targeting AD and ageing pathways. We have also identified a robust mitophagy inducer which passes the blood-brain barrier and inhibits AD pathologies in mice and a 3D mini-brain system (unpublished data). TheFang lab is now involved in several clinical trials looking into the use of NAD⁺ precursors to treat AD and premature ageing diseases, among others.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Miss Angela Wong at 3917 9216.