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.
The aqueous ethanolic extract of the marine plant Thalassia testudinum, named BM-21, has powerful antioxidant and antilipoperoxidative activities. The extract also has anti-inflammatory, antinociceptive and neuroprotective effect against acrylamide-induced neurotoxicity. Excessive generation of free radicals and decreased levels of the antioxidant enzymes have been observed either during the brain ischemia or following reperfusion. In the present work we studied the neuroprotective potential of BM-21 against brain damage induced by transient bilateral carotid artery occlusion model of global cerebral ischemia in Mongolian gerbils. Oral administration of BM-21 (400 mg/kg, once a day for 8 days) prior to ischemic insult provides significant neuroprotection with respect to mortality, neurological symptoms, infarct volume and brain edema after. We also found that BM-21 reduces hippocampal neuronal death in the CA1 region and attenuates the increase of lipid peroxidation products (MDA). The extract also improves the activity of SOD and GSHPx and increases the content of GSH in brain homogenates. BM-21 administered at a dose at which the extract showed to be effective as anti-ischemic agent in vivo also reduces susceptibility of brain homogenates of non-ischemic gerbils against metal and non-metal lipid peroxidation in vitro. Taken
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