Guojun Bu, United States of America

Mayo Clinic Department of Neuroscience
Dr. Guojun Bu is the Chair of the Department of Neuroscience at Mayo Clinic Jacksonville. He holds the academic rank of Mary Lowell Leary Professor of Medicine and Professor of Neuroscience. Dr. Bu is also the Jorge and Leslie Bacardi Associate Director of the Mayo Clinic Center for Regenerative Medicine and an Associate Director of the Mayo Clinic Alzheimer’s Disease Research Center. Prior to joining Mayo Clinic in 2010, he was a Professor of Cell Biology and Neuroscience at the Washington University School of Medicine in St. Louis. Dr. Bu received his B.S. degree in biology from Beijing Normal University, his Ph.D. degree in biochemistry from Virginia Tech, and completed his postdoctoral training in cell biology at the Washington University School of Medicine. Dr. Bu is a world leader in the field of apoE and apoE receptors, which play critical roles in the pathogenesis of Alzheimer’s disease. His primary interest is to understand why APOE4 is a strong genetic risk factor for Alzheimer’s disease and how this pathway can be targeted for therapy by studying animal and stem cell-based cellular and organoid models. His research also includes interests in addressing the pathobiology of TREM2 and the glial and vascular contributions to Alzheimer’s disease and related dementias. Dr. Bu has received numerous honors and awards including the Zenith Fellows Award from the Alzheimer’s Association, the Established Investigator Award from the American Heart Association, the Investigator of the Year award from the Mayo Clinic, and the MetLife Foundation Award for Medical Research in Alzheimer’s disease. He is an elected Fellow of the American Association for the Advancement of Science (AAAS), a Co-Editor-in-Chief of Molecular Neurodegeneration and an Associate Editor for Science Advances.

Moderator of 1 Session

LIVE SYMPOSIUM DISCUSSION

LIVE DISCUSSION - TREM2 AND TREM 1 (2)

Date
11.03.2021, Thursday
Session Time
17:30 - 18:00
Session Icon
Live

Presenter of 8 Presentations

APOE2 AND RARE PROTECTIVE VARIANTS AGAINST ALZHEIMER’S DISEASE: HOW DO THEY DO IT?

Session Type
PRE CONFERENCE SYMPOSIUM
Date
09.03.2021, Tuesday
Session Time
10:00 - 14:50
Room
Pre-Conference 1
Lecture Time
12:30 - 12:50
Session Icon
On-Demand and Live Q&A

WELCOME AND INTRODUCTION INCLUDING WORKSHOP GENERAL DISCUSSION PRIMER

Session Type
PRE CONFERENCE SYMPOSIUM
Date
09.03.2021, Tuesday
Session Time
10:00 - 14:50
Room
Pre-Conference 1
Lecture Time
10:00 - 10:30
Session Icon
On-Demand and Live Q&A

APOE AND TREM2: ZOOMING IN ON CONVERGING MICROGLIAL RESPONSES IN ALZHEIMER’S DISEASE

Session Type
PLENARY LECTURE
Date
12.03.2021, Friday
Session Time
07:30 - 08:00
Room
Plenary
Lecture Time
07:31 - 08:00
Session Icon
On-Demand

Abstract

Abstract Body

The APOE gene is the strongest genetic risk factor for Alzheimer’s disease (AD) with APOE4 strongly increases the risk by driving amyloid pathology, although several amyloid-β (Aβ)-independent pathways such as impaired lipid metabolism and compromised cerebrovascular function also contribute. Studies from our group and others have identified apoE, phospholipids, and Aβ as ligands for TREM2, a microglia-specific gene in the brain with its variants also strongly linked to AD risk. To further address the molecular mechanisms underlying apoE- and TREM2-related AD risk, we generated conditional mouse models expressing human APOE3 or APOE4 specifically in microglia in the murine Apoe knockout background. Similar mouse models were also generated for the common allele TREM2 or AD-risk associated TREM2-R47H. In the absence of amyloid pathology, we observed enhanced synaptic functions and behaviors, as well as microglial responses to acute injury, by apoE3 and TREM2, but not apoE4 or TREM2-R47H. In the presence of amyloid pathology, both apoE4 and TREM2-R47H exhibited loss-of-function effects in microglial clustering around the amyloid plaques associated with reduced amyloid pathology compared with apoE3 or TREM2, respectively. Molecular profiling by single cell RNA-sequencing revealed apoE isoform- or TREM2-specific pathways underlying differential microglial functions and their responses to amyloid pathology. Interestingly, we found that apoE expression is highly modulated by TREM2, suggesting that apoE is functionally downstream of TREM2. Together, our studies define critical roles of apoE and TREM2 in microglial functions, establishing a common neuroimmune pathway modulated by the two strong genetic risk factors for AD.

Hide

APOE AND TREM2 IN MICROGLIAL FUNCTIONS AND ALZHEIMER’S DISEASE

Session Type
LIVE- MEET THE PROFESSOR
Date
10.03.2021, Wednesday
Session Time
16:30 - 17:30
Room
Meet The Prof A
Lecture Time
16:30 - 17:30
Session Icon
Live

LIVE DISCUSSION & Q&A: HOW DOES RESILIENCE, FROM GENETICS TO ENVIRONMENTAL, AT THE CELLULAR, SYSTEMS, OR POPULATION LEVELS, PLAY A ROLE IN REDUCING RISK FOR NEURODEGENERATIVE DISEASE?