School of Biomedical Sciences cordially invites you to join the following seminar:

Speaker: Dr. Evandro Fei Fang, Associate Professor, University of Oslo and Akershus University Hospital, Norway
Talk Title: Fine-tuning the NAD+-mitophagy axis in healthy brain ageing and the use of AI in related drug development

Date: 27 February 2025 (Thursday)
Time: 4:00 pm – 5:00 pm
Venue: Seminar Room 2, G/F, Laboratory Block, 21 Sassoon Road
Host: Professor Shoutang Wang

Biography

Evandro F. Fang is an Associate Professor of Molecular Gerontology at the University of Oslo (UiO, Norway), and his group are working on the molecular mechanisms of human ageing and age-predisposed neurodegeneration (https://evandrofanglab.com), with a special focus on NAD+ and mitophagy in neuronal resilience. He has published over 100 papers in international peer-reviewed journals including papers in Cell, Cell Metabolism, Nature Reviews MCB, Nature Neuroscience, Nature Ageing, Nature Biomedical Engineering, and Lancet Healthy Longevity. He routinely reviews grants for more than 30 leading foundations, including ERC (EU), MRC (UK), and many in Hong Kong. He has received several awards including the 2023 Norwegian National Dementia research award of the National Association for Public Health presented by H.M. King Harald V of Norway.

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); 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. Mitophagy is the cellular self-clearing process that removes damaged and superfluous mitochondria, playing a fundamental role in maintaining neuronal homeostasis and survival. We hypothesise that age-susceptible defective mitophagy causes accumulation of damaged mitochondria, first in the high energy-demanding and ‘fragile’ entorhinal cortex Layer II region, leading to inflammation, senescence, and finally cellular dysfunction and/or death; this age-related risk combines with genetic and environmental risks causing AD and its progression. Mitophagy/autophagy restoration, through pharmaceutical (e.g., NAD+, passion fruit components, and urolithin A) and genetic approaches, forestalls pathology and cognitive decline in AD animal models and improves function of AD iPSC-derived neurons. Additionally, AI is now being used to propel drug screening and design specifically targeting AD and ageing. The Evandro Fang lab is now leading/involved in several clinical trials looking into the use of NAD+ precursors to treat AD and premature ageing diseases, among others.

ALL ARE WELCOME.