Guojun Bu, Ph.D.

Professor of Neuroscience, Mayo Clinic Jacksonville;

Editor-in-Chief, Molecular Neurodegeneration

Guojun Bu, Ph.D., is a Professor of Neuroscience at Mayo Clinic Jacksonville. Prior to joining Mayo Clinic in 2010, he was a Professor in Cell Biology and Neuroscience in the Washington University School of Medicine in St. Louis. Dr. Bu received his B.S. degree in biology from Beijing Normal University and his Ph.D. degree in biochemistry from Virginia Tech. He is a leader in the field of apoE and apoE receptors, which play critical roles in the pathogenesis of Alzheimer’s disease (AD). His primary interest is to understand why APOE4 is a strong genetic risk factor for AD and how this pathway can be targeted for therapy. His laboratory is also exploring the potentials of human skin fibroblast-derived stem cells in the replacement of lost neurons and blood vessels in AD and vascular dementia. Dr. Bu has received several honors and awards including the Faculty Scholar Award and the Zenith Fellows Award from the Alzheimer’s Association and the Established Investigator Award from the American Heart Association. He is the Editor-in-Chief of Molecular Neurodegeneration and serves in review panels for the National Institutes of Health and the BrightFocus Foundation.

Funded Research

Project Description Researchers Funding
ABCA7 in Brain Homeostasis and Alzheimer's Disease

Genetic and environmental risk factors contribute to the etiology of late-onset Alzheimer's disease (LOAD), which accounts for vast majority of disease cases. In addition to APOE, recent genome-wide association studies have identified novel susceptibility genes for LOAD. Among them, gene variants in ABCA7 coding ATP-binding cassette transporter A7 (ABCA7), which is a homologous transmembrane protein to ABCA1, have shown strong association with the increased risk for LOAD.

2015
$200,000
Vascular Regenerative Therapy for Alzheimer’s Disease

Alzheimer’s disease (AD) is a major cause of dementia in elderly. The amyloid-β (Aβ) peptides deposit in the brain parenchyma as senile plaques and in the cerebrovasculature as cerebral amyloid angiopathy (CAA), both are hallmarks of AD pathology. Epidemiologically, cerebrovascular damages caused by diabetes mellitus or stroke increase the risk for AD. Cerebral hypoperfusion precedes cognitive decline and neurodegeneration in AD. Our recent work has also demonstrated that cerebrovasculature plays critical roles in Aβ clearance.

2013
$100,000

Selected Publications

These published papers resulted from Cure Alzheimer’s Fund support.
Atagi Y, Liu CC, Painter MM, Chen XF, Verbeeck C, Zheng H, Li X, Rademakers R, Kang SS, Xu H, Younkin S, Das P, Fryer JD, Bu G, Apolipoprotein E Is a Ligand for Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), The Journal of Biological Chemistry, 290(43), Oct 2015, 26043-50
, Casey CS, Atagi Y, Yamazaki Y, Shinohara M, Tachibana M, Fu Y, Bu G, Kanekiyo T, Journal of Biological Chemistry, 290(22), May 2015, 14208-14217
Chia-Chen Liu, Jin Hu, Chih-Wei Tsai, Mei Yue, Heather L. Melrose, Takahisa Kanekiyo, and Guojun Bu, Neuronal LRP1 Regulates Glucose Metabolism and Insulin Signaling in the Brain, The Journal of Neuroscience, 35(14), April 2015, 5851-5859