Ontology highlight
ABSTRACT:
SUBMITTER: Liu CC
PROVIDER: S-EPMC8824726 | biostudies-literature | 2021 Sep
REPOSITORIES: biostudies-literature
Liu Chia-Chen CC Murray Melissa E ME Li Xia X Zhao Na N Wang Na N Heckman Michael G MG Shue Francis F Martens Yuka Y Li Yonghe Y Raulin Ana-Caroline AC Rosenberg Cassandra L CL Doss Sydney V SV Zhao Jing J Wren Melissa C MC Jia Lin L Ren Yingxue Y Ikezu Tadafumi C TC Lu Wenyan W Fu Yuan Y Caulfield Thomas T Trottier Zachary A ZA Knight Joshua J Chen Yixing Y Linares Cynthia C Wang Xue X Kurti Aishe A Asmann Yan W YW Wszolek Zbigniew K ZK Smith Glenn E GE Vemuri Prashanthi P Kantarci Kejal K Knopman David S DS Lowe Val J VJ Jack Clifford R CR Parisi Joseph E JE Ferman Tanis J TJ Boeve Bradley F BF Graff-Radford Neill R NR Petersen Ronald C RC Younkin Steven G SG Fryer John D JD Wang Hu H Han Xianlin X Frieden Carl C Dickson Dennis W DW Ross Owen A OA Bu Guojun G
Science translational medicine 20210929 613
Apolipoprotein E (<i>APOE</i>) genetic variants have been shown to modify Alzheimer’s disease (AD) risk. We previously identified an <i>APOE3</i> variant (<i>APOE</i>3-V236E), named <i>APOE3</i>-Jacksonville (<i>APOE3</i>-Jac), associated with healthy brain aging and reduced risk for AD and dementia with Lewy bodies (DLB). Herein, we resolved the functional mechanism by which APOE3-Jac reduces APOE aggregation and enhances its lipidation in human brains, as well as in cellular and biochemical as ...[more]