Cholesterol paradox: Is high total or low HDL cholesterol level a risk for Alzheimer's disease?
Article first published online: 25 FEB 2003
Copyright © 2003 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 72, Issue 2, pages 141–146, 15 April 2003
How to Cite
Michikawa, M. (2003), Cholesterol paradox: Is high total or low HDL cholesterol level a risk for Alzheimer's disease?. J. Neurosci. Res., 72: 141–146. doi: 10.1002/jnr.10585
- Issue published online: 27 MAR 2003
- Article first published online: 25 FEB 2003
- Manuscript Accepted: 6 JAN 2003
- Manuscript Received: 3 JAN 2003
- Comprehensive Research on Aging and Health, Ministry of Health, Labor, and Welfare, Japan
- Program for Promotion of Fundamental Studies in Health Sciences of the Organization for Pharmaceutical Safety and Research of Japan
- Alzheimer's disease;
- amyloid cascade;
- amyloid β-protein;
- apolipoprotein E
Cholesterol is an essential component of membranes for maintaining their structure and functions. The discovery that possession of apolipoprotein E (apoE), allele ϵ4 is a strong risk factor for Alzheimer's disease (AD) leads us to focus on the role of cholesterol in the pathogenesis of AD. Accumulating epidemiological and biological evidence suggests the link between the serum cholesterol level and the development of AD, and the potential therapeutic effectiveness of statins for AD and mild cognitive impairment (MCI), whereas other lines of evidence show controversial results. Cholesterol is known to interact with amyloid β-protein (Aβ) in a reciprocal manner: cellular cholesterol levels modulate Aβ generation, whereas Aβ alters cholesterol dynamics in neurons, leading to tauopathy. In this review, the relationship between the cholesterol levels in serum or cerebrospinal fluid (CSF) and the induction of AD is discussed. The mechanism(s), if this is the case, of how cholesterol in the central nervous system (CNS) is involved in the induction of pathologies of AD including Aβ generation and tauopathy, and how statins prevent it are also discussed. © 2003 Wiley-Liss, Inc.