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A more recent version of this article appeared on May 1, 2005

Papers In Press, published online ahead of print February 16, 2005
J. Lipid Res., doi:10.1194/jlr.M400486-JLR200
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Submitted on December 10, 2004
Revised on February 15, 2005
Accepted on February 15, 2005

Lipid homeostasis and apolipoprotein E in the development and progression of Alzheimer's disease

Roger M. Lane and Martin R. Farlow

Novartis Neuroscience, CDMA, Novartis Pharmaceuticals Corporation, East Hanover, NJ 07936-1080

Corresponding Author: roger.lane{at}pharma.novartis.com

Extracellular amyloid plaques, intracellular neurofibrillary tangles, and loss of basal forebrain cholinergic neurons in the brains of Alzheimer's disease (AD) patients may be the end result of abnormalities in lipid metabolism and peroxidation that may be due to, or exacerbated by, beta-amyloid peptide (Aß). Apolipoprotein E (apoE) is a major apolipoprotein in the brain, mediating transport and clearance of lipids and Aß. ApoE-dependent dendritic and synaptic regeneration may be less efficient with apoE4, and this may result in, or unmask, age-related neurodegenerative changes. The increased risk of AD associated with apoE4 may be modulated by diet, vascular risk factors, and genetic polymorphisms that affect the function of other transporter proteins and enzymes involved in brain lipid homeostasis. Diet and apoE lipoproteins influence membrane lipid raft composition and properties of enzymes, transporter proteins, and receptors mediating Aß production and degradation, tau phosphorylation, glutamate and glucose uptake, and neuronal signal transduction. The level and isoform of apoE may influence whether Aß is likely to be metabolized or deposited. This review examines current evidence for diet, lipid homeostasis, and apoE in the etiology of AD. Effects on the cholinergic system and response to cholinesterase inhibitors by APOE allele carrier status are briefly discussed.


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