G
Guojun Bu
Researcher at Mayo Clinic
Publications - 360
Citations - 31640
Guojun Bu is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Apolipoprotein E & LDL receptor. The author has an hindex of 91, co-authored 313 publications receiving 25684 citations. Previous affiliations of Guojun Bu include Washington University in St. Louis & Xiamen University.
Papers
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Journal ArticleDOI
Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy
TL;DR: The A β-dependent and Aβ-independent mechanisms that link Apo-E4 status with AD risk are discussed, and how to design effective strategies for AD therapy by targeting ApO-E is considered.
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Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy
TL;DR: There is mounting evidence that APOE4 contributes to AD pathogenesis by modulating the metabolism and aggregation of amyloid-β peptide and by directly regulating brain lipid metabolism and synaptic functions through APOE receptors.
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Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease
TL;DR: There is substantial evidence that differential effects of apoE isoform on AD risk are influenced by the ability of apOE to affect Aβ aggregation and clearance in the brain.
Journal ArticleDOI
Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies
TL;DR: Increasing evidence suggests that the effect of APOE*ε4 on AD risk is exerted through inhibition of amyloid-β (Aβ) clearance and promotion of Aβ aggregation, although the relevance of this observation to AD pathogenesis requires further investigation.
Journal ArticleDOI
Endocytosis Is Required for Synaptic Activity-Dependent Release of Amyloid-β In Vivo
John R. Cirrito,Jae Eun Kang,Jiyeon Lee,Floy R. Stewart,Deborah K. Verges,Luz M. Silverio,Guojun Bu,Steven Mennerick,David M. Holtzman +8 more
TL;DR: It is estimated that approximately 70% of ISF Abeta arises from endocytosis-associated mechanisms, with the vast majority of this pool also dependent on synaptic activity, which has implications for AD pathogenesis and may provide insights into therapeutic intervention.