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Current Trends in Neurology   Volumes    Volume 1 
Abstract
Lipid abnormalities and neural dysfunction: hypercholesterolemia and lipoprotein lipase deficiency
Pierre Julien, Nathalie Laflamme, M. R. Ven Murthy
Pages: 21 - 36
Number of pages: 16
Current Trends in Neurology
Volume 1 

Copyright © 2005 Research Trends. All rights reserved

ABSTRACT
 
Brain must have a continuous supply of cholesterol and essential fatty acids for its normal function. Cholesterol is furnished either by de novo synthesis or by uptake of extracellular cholesterol through cell receptors. Removal of excess cell cholesterol is mainly controlled by the formation of brain specific 24S-hydroxycholesterol (24S-OHchol), also called cerebrosterol, produced by the neuronal oxidative enzyme CYP46. Disturbances in cholesterol homeostasis resulting in the accumulation of 24S-OHchol have been demonstrated to lead to brain disorders such as Alzheimer’s disease (AD). It has recently been shown that inhibitors of cholesterol synthesis, statins, can reduce plasma concentrations of 24S-OHchol in AD patients. However, it is unknown if inhibition of cholesterol synthesis by statins could also have detrimental effects on the establishment and maintenance of new synaptic connections in the brains of patients with neurodegenerative disorders.
 
Lipoprotein lipase (LPL) is the key enzyme involved in the hydrolysis of triglycerides and supply of fatty acids to various tissues. The nutritional essential polyunsaturated fatty acids(PUFAs), such as docosahexaenoic acid (DHA) and arachidonic acid (AA) are major components of the brain and critical to brain maturation and functions. Reduction in n-3 PUFAs has been correlated to major depression in patients associated with or without coronary artery disease. Reports have emphasized the role of PUFAs  in  numerous neuropathologies; however, the function of LPL in the central nervous system (CNS) remains to be clarified. Recently, we have published new observations on the role of LPL in neurite maturation and in brain response to ischemia. We now report reduction in the plasma of n-3 PUFAs in patients with LPL deficiency and discuss its significance in relation to the role of LPL in the brain tissue.
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