Apolipoprotein E as a β-amyloid-independent factor in Alzheimer's disease

被引：0

作者：

Wolf A.B. ^{[1
]}

Valla J. ^{[2
,3
]}

Bu G. ^{[4
]}

Kim J. ^{[4
]}

Ladu M.J. ^{[5
]}

Reiman E.M. ^{[3
,6
,7
,8
]}

Caselli R.J. ^{[3
,9
]}

机构：

[1] Medical Scientist Training Program, University of Colorado Anschutz Medical Campus, Mail Stop B176, Aurora, CO 80045

[2] Department of Biochemistry, Midwestern University, Glendale, AZ 85308

[3] Arizona Alzheimer's Consortium, Phoenix, AZ

[4] Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224

[5] Department of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612

[6] Banner Alzheimer's Institute, Banner Good Samaritan PET Center, Phoenix, AZ 85006

[7] Neurogenomics Division, Translational Genomics Research Institute (TGen), Phoenix, AZ 85004

[8] Department of Psychiatry, University of AZ, Phoenix, AZ 85004

[9] Department of Neurology, Mayo Clinic Arizona, Scottsdale, AZ 85259

来源：

Alzheimer's Research & Therapy | / 5卷 / 5期

关键词：

Cerebral Amyloid Angiopathy; Cerebral Metabolic Rate; apoE Isoforms; Human apoE4; apoE4 Mouse;

D O I：

10.1186/alzrt204

中图分类号：

学科分类号：

摘要：

APOE, which encodes apolipoprotein E, is the most prevalent and best established genetic risk factor for late-onset Alzheimer's disease. Current understanding of Alzheimer's disease pathophysiology posits an important role for apolipoprotein E in the disease cascade via its interplay with β-amyloid. However, evidence is also emerging for roles of apolipoprotein E in the disease process that are independent of β-amyloid. Particular areas of interest are lipid metabolism, tau pathology, neuroenergetics, neurodevelopment, synaptic plasticity, the neurovasculature, and neuroinflammation. The intent of this article is to review the literature in each of these areas. © 2013 BioMed Central Ltd.

引用

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