Abstract
The knockout mouse model, B6.129P2-Apoetm1Unc is homozygotic for the Apolipoprotein E (ApoE) deletion; thus, it is capable of developing hyperlipidemia and atherosclerosis but ApoE is also a lipid-transport protein abundantly expressed in most neurons in the central nervous system, so these animals could also be models of neurodegenerative diseases. The aim of this study was to determine age-related changes in spontaneous behavior and in learning and memory of Apolipoprotein E knockout mice. Spontaneous behavioral measurements included sleeping pattern, motor coordination and balance by rotarod and open field activity, whereas learning and memory tests included forced alternation in Y-maze, novel object recognition and passive avoidance conditioning. Significant behavioral differences between aged knockout mice and age-matched wild type strain, C57Bl/6 were found in all the behavioral tests, except for the rotarod test. Genetically’ modified mice exhibited less huddling contact during sleeping, decreased locomotor activity in novel environments and in learning and memory deficits. These results are consistent with the cognitive impairment and memory loss seen as the earliest clinical symptoms in neurodegenerative disorders such as Alzheimer’s disease. The ApoE knockout mice might therefore be an appropriate model for studying the underlying mechanisms involved in behavioral changes caused by neurodegenerative diseases as well as for evaluating new therapies for these pathologies.
Highlights
Apolipoprotein (Apo) E had been recognized as a critical protein constituent of lipoproteins, with important functions in controlling lipoprotein metabolism and cholesterol homeostasis.This protein participates in the transport of plasma lipids and in the redistribution of lipids among cells [1].Emerging study has shown that Apolipoprotein E (ApoE) and ApoE isoform functions may extend beyond lipid metabolism, to include maintenance of normal brain function [2]
Emerging study has shown that ApoE and ApoE isoform functions may extend beyond lipid metabolism, to include maintenance of normal brain function [2]
Apolipoprotein E is expressed in the central and peripheral nervous systems [3]; produced and secreted mainly by astrocytes [4], ApoE is a major carrier of cholesterols that are required for neuronal activity and injury repair in the brain, so it is probably involved in the removal of debris from damaged cells and in the stimulation of nerve cell regeneration [5]
Summary
Apolipoprotein (Apo) E had been recognized as a critical protein constituent of lipoproteins, with important functions in controlling lipoprotein metabolism and cholesterol homeostasis.This protein participates in the transport of plasma lipids and in the redistribution of lipids among cells [1].Emerging study has shown that ApoE and ApoE isoform functions may extend beyond lipid metabolism, to include maintenance of normal brain function [2]. Apolipoprotein (Apo) E had been recognized as a critical protein constituent of lipoproteins, with important functions in controlling lipoprotein metabolism and cholesterol homeostasis. This protein participates in the transport of plasma lipids and in the redistribution of lipids among cells [1]. Emerging study has shown that ApoE and ApoE isoform functions may extend beyond lipid metabolism, to include maintenance of normal brain function [2]. Apolipoprotein E is expressed in the central and peripheral nervous systems [3]; produced and secreted mainly by astrocytes [4], ApoE is a major carrier of cholesterols that are required for neuronal activity and injury repair in the brain, so it is probably involved in the removal of debris from damaged cells and in the stimulation of nerve cell regeneration [5].
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