|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From the Gladstone Institute of Neurological Disease, the Gladstone Institute of Cardiovascular Disease, and the Departments of Pathology and Neurology, University of California, San Francisco, CA.
Address correspondence and reprint requests to Dr. Yadong Huang, Gladstone Institute of Neurological Disease, 1650 Owens Street, San Francisco, CA 94158; e-mail: yhuang{at}gladstone.ucsf.edu
Apolipoprotein (apo) E, a multifunctional protein with central roles in lipid metabolism and neurobiology, has three common isoforms (apoE2, apoE3, and apoE4) with different effects on lipid homeostasis and neurobiology. Unlike apoE3, the most common isoform, apoE4, is associated with increased risk of developing Alzheimer disease (AD) and other neurodegenerative disorders. Although the mechanisms underlying apoE4's action in AD pathogenesis are still poorly understood, emerging data strongly suggest that apoE4 contributes to this disease by interacting with different factors through various pathways. Thus, multiple molecular and cellular mechanisms should be considered when anti-AD drugs are developed based on apoE studies.
This article was previously published in electronic format as an Expedited E-Pub at www.neurology.org.
Supported by National Institutes of Heath Grants P01 AG022074 and R01 HL037063.
Disclosure: The author reports no conflicts of interest.
Received June 22, 2005. Accepted in final form October 14, 2005.
This article has been cited by other articles:
![]() |
E. E. Benarroch Brain cholesterol metabolism and neurologic disease Neurology, October 21, 2008; 71(17): 1368 - 1373. [Full Text] [PDF] |
||||
![]() |
Q. Xu, D. Walker, A. Bernardo, J. Brodbeck, M. E. Balestra, and Y. Huang Intron-3 Retention/Splicing Controls Neuronal Expression of Apolipoprotein E in the CNS J. Neurosci., February 6, 2008; 28(6): 1452 - 1459. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Brodbeck, M. E. Balestra, A. M. Saunders, A. D. Roses, R. W. Mahley, and Y. Huang Rosiglitazone increases dendritic spine density and rescues spine loss caused by apolipoprotein E4 in primary cortical neurons PNAS, January 29, 2008; 105(4): 1343 - 1346. [Abstract] [Full Text] [PDF] |
||||
![]() |
X. He, K. Cooley, C. H. Y. Chung, N. Dashti, and J. Tang Apolipoprotein Receptor 2 and X11{alpha}/{beta} Mediate Apolipoprotein E-Induced Endocytosis of Amyloid-{beta} Precursor Protein and {beta}-Secretase, Leading to Amyloid-{beta} Production J. Neurosci., April 11, 2007; 27(15): 4052 - 4060. [Abstract] [Full Text] [PDF] |
||||
![]() |
Q. Xu, A. Bernardo, D. Walker, T. Kanegawa, R. W. Mahley, and Y. Huang Profile and Regulation of Apolipoprotein E (ApoE) Expression in the CNS in Mice with Targeting of Green Fluorescent Protein Gene to the ApoE Locus. J. Neurosci., May 10, 2006; 26(19): 4985 - 4994. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. E. Finch A perspective on sporadic inclusion-body myositis: The role of aging and inflammatory processes Neurology, January 24, 2006; 66(1_suppl_1): S1 - S6. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |