Introduction

A model for cholesterol transport and homeostasis within the central nervous system has been proposed by Pitas et al. (1987) after the visualization by immunocytochemistry in rat and monkey brains of the presence of a low-density lipoprotein (LDL) receptor. Apolipoprotein (apo) E and apoAJcontaining particles were also detected in human cerebrospinal fluid (Pitas et al., 1987). Furthermore, enzymes involved in lipid metabolism have been located within the brain: LCAT mRNA has been shown to be expressed in rat brains, cholesteryl ester transfer protein which plays a key role in cholesterol homeostasis has been detected in human cerebrospinal fluid and seems to be synthesized in the brain (Albers et al., 1992). The distribution of the low-density lipoprotein receptor-related protein (LRP), a multifunctional receptor that binds apoE, is highly restricted and limited to the grey matter, primarily associated with neuronal cell population (Wolf et al., 1992). The difference in cellular expression of ligand (apoE) and receptor (LRP) may provide a pathway for intracellular transport of apoEcontaining lipoproteins in the central nervous system. All these data leave little doubt that the brain is equipped with a relatively self-sufficient transport system for cholesterol.