Department of Neuroscience, Center for Translational Research in Neurodegenerative Disease, McKnight Brain Institute, University of Florida, Gainesville, Florida, USA.
Address correspondence to: David R. Borchelt, Department of Neuroscience/CTRND, Box 100159, 1275 Center Drive, University of Florida, Gainesville, Florida 32610, USA. Phone: 352.273.9664; Email: firstname.lastname@example.org.
First published March 30, 2018 - More info
See the related article at Targeting of nonlipidated, aggregated apoE with antibodies inhibits amyloid accumulation.
Inheritance of the E4 allele of the apolipoprotein E gene (APOE4) substantially increases the risk of developing late-onset Alzheimer disease (AD). A large body of evidence has firmly established a role for apoE in modulating the risk of developing the amyloid plaque pathology that is pathognomonic for AD. In this issue of the JCI, Liao and colleagues discovered that antibodies against a nonlipidated form of apoE4 are highly effective in delaying the deposition of amyloid β (Aβ) peptides in mouse models of AD pathology. Using a combination of passive immunization and viral-mediated expression of recombinant antibodies, the authors show that Fc receptor–mediated clearance of the nonlipidated apoE4 was critical in delaying Aβ deposition. Collectively, this study identifies a new therapeutic target that could be exploited to prevent, or possibly reverse, the Aβ pathology of AD.
A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.
Click here to sign into your account.
Please select one of the subscription options, which includes a low-cost option just for this article.
If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).
Please try these troubleshooting tips.