Targeting on Mitophagy and NAD+ to Extend Human Healthspan and Lifespan | Duke Kunshan University
Targeting on Mitophagy and NAD+ to Extend Human Healthspan and Lifespan
Speaker: 
Dr. Evandro F. Fang

Group leader/Assistant Professor, Department of Clinical Molecular Biology, University of Oslo Akershus University Hospital, Norway

Apr 16th 2019 12:00 to 13:00
Room 3107, Academic Building
Tuesday, April 9, 2019 - 10:30

Summary of talk:     

There were 962 million elderly (60+) globally in 2017, and this number will rise to 2.1 billion in 2050, bringing formidable healthcare and socio-economic challenges. Aging is arguably the highest risk factor for numerous human diseases, thus understanding the molecular mechanisms of human aging holds the promise to develop interventional and therapeutic strategies for many diseases all at once, promoting healthy longevity.

Accumulation of damaged mitochondria is a hallmark of human aging and age-related neurodegeneration, including Alzheimer’s disease (AD). However, the molecular mechanisms of the impaired mitochondrial homeostasis and their relationship to AD are still elusive. Mitophagy is a cellular self-clearing process of damaged and superfluous mitochondria, thereby plays a fundamental role in maintaining neuronal function and survival. We hypothesize that defective mitophagy causes accumulation of damaged mitochondria, which further in combination with the two main AD causative factors, Aβ plaques and tau tangles, exacerbating AD progression. Restoration of mitophagy through upregulation of cellular NAD+, a primary cofactor in human health and life, forestalls pathology and cognitive decline in C. elegans and mouse models of AD. In view of the physiological feature of NAD+ in human, our study suggests immediate interventional/therapeutic potential for both normal ageing and age-related memory loss. 

Brief Biography:

Dr. Evandro F. Fang is investigating the molecular mechanisms of one of the most fundamental and fascinating topics in current biology: human aging. After finished his Ph.D training in Biochemistry at the Chinese University of Hong Kong in 2012, he started a 5-year postdoctoral fellowship at the National Institute on Aging USA with Dr. Vilhelm Bohr. In September 2017, he established his independent laboratory at the University of Oslo, Norway. His laboratory is focused on the molecular mechanisms of how cells clear their damaged and aged mitochondria, a process called “mitophagy”, as well as the roles of mitophagy in Alzheimer’s disease. He is fascinated with and actively engaged in moving his laboratory findings to translational applications, with the overarching goal to establish novel and safe biological approaches to promote longer and healthier human lives.

He has published over 55 papers in peer-reviewed journals including papers in Cell, Cell Metabolism, Nature Reviews MCB, and Nature Neuroscience. He has received several awards including The NIH Fellows Award for Research Excellence 2014, 2015, and an awardee of the prestigious Butler-Williams Scholar on Aging 2016 (USA), an FRIMEDBIO Young Research Talent 2017(Norway), and a finalist of the 2017 ERC Starting grant.