Human apoE Isoforms Differentially Regulate Brain Amyloid-β Peptide Clearance

Joseph M. Castellano1,2,3, Jungsu Kim1,2,3, Floy R. Stewart1,2,3, Hong Jiang1,2,3, Ronald B. DeMattos4, Bruce W. Patterson5, Anne M. Fagan1,2,3, John C. Morris1,2, Kwasi G. Mawuenyega1,2,3, Carlos Cruchaga1,6,3, Alison Goate1,2,6,3, Kelly R. Bales7, Steven M. Paul8, Randall J. Bateman1,2,3, David M. Holtzman1,9,2,3
1Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
2Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
3Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA
4Eli Lilly and Co., Lilly Research Labs, Indianapolis, IN 46285, USA.
5Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, 63110, USA
6Department of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA.
7Neuroscience Research Unit, Pfizer Global Research & Development, Groton, CT 06430, USA.
8Appel Alzheimer’s Disease Research Institute, Weill Cornell Medical College, Cornell University, New York, NY 10065, USA.
9Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO, 63110, USA

Tóm tắt

Human apoE4 increases the concentration of soluble Aβ in the brain by impairing its clearance.

Từ khóa


Tài liệu tham khảo

10.1126/science.1072994

10.1126/science.8346443

10.1212/WNL.43.8.1467

10.1038/ng0694-180

10.1016/S1474-4422(10)70325-2

10.1073/pnas.0900345106

10.1002/ana.21843

10.1073/pnas.90.20.9649

10.1212/01.WNL.0000128091.92139.0F

10.1073/pnas.050004797

10.1006/nbdi.2002.0483

10.1073/pnas.0409072102

10.1523/JNEUROSCI.5170-04.2005

10.1523/JNEUROSCI.0887-09.2009

10.1212/01.wnl.0000261919.22630.ea

10.1093/brain/awm336

10.1002/ana.21610

10.1002/ana.20730

10.1001/archneur.64.3.noc60123

10.1001/jama.289.16.2094

10.1001/archneur.60.12.1696

10.1002/ana.21559

10.1002/ana.20009

10.1093/brain/awn016

10.1001/archneur.65.10.noc80013

10.1001/archneurol.2008.596

10.1212/01.wnl.0000228230.26044.a4

10.1038/ng1197-263

10.1523/JNEUROSCI.23-26-08844.2003

10.1523/JNEUROSCI.2637-09.2009

10.1016/j.neuron.2009.11.013

10.1016/S0896-6273(03)00850-X

10.1021/ac00030a003

10.3171/jns.2001.94.3.0397

10.1089/neu.2005.22.3

10.1126/science.1161591

10.1016/j.nbd.2010.06.018

10.1126/science.1180962

10.1016/j.neuron.2009.06.026

10.1371/journal.pone.0018850

Wahrle S. E., Jiang H., Parsadanian M., Kim J., Li A., Knoten A., Jain S., Hirsch-Reinshagen V., Wellington C. L., Bales K. R., Paul S. M., Holtzman D. M., Overexpression of ABCA1 reduces amyloid deposition in the PDAPP mouse model of Alzheimer disease. J. Clin. Invest. 118, 671–682 (2008).

10.1006/nbdi.1995.0019

10.1038/nm1438

10.1038/454418a

10.1038/nature08538

10.1146/annurev.med.47.1.387

10.1038/372092a0

Wisniewski T., Castano E. M., Golabek A., Vogel T., Frangione B., Acceleration of Alzheimer’s fibril formation by apolipoprotein E in vitro. Am. J. Pathol. 145, 1030–1035 (1994).

10.1097/00001756-199810050-00031

10.1021/bi961074j

10.1016/S0021-9258(17)31529-6

10.1046/j.1471-4159.1997.68020721.x

10.1021/bi9626362

10.1042/bj3480359

10.1038/sj.jcbfm.9600419

10.1172/JCI36663

10.1073/pnas.0604011103

10.1046/j.1471-4159.1998.70041458.x

10.1016/S0306-4522(98)00561-2

10.1016/j.neuron.2008.04.010

10.1186/1750-1326-4-21

10.1074/jbc.M502143200

10.1523/JNEUROSCI.1972-08.2008

10.1016/j.jmb.2008.12.040

10.1126/science.1197623