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Mini-Review Article

Cerebrovascular Changes and Neurodegeneration Related to Hyperlipidemia: Characteristics of the Human ApoB-100 Transgenic Mice

[ Vol. 26 , Issue. 13 ]

Author(s):

Melinda E. Tóth*, Brigitta Dukay , Zsófia Hoyk and Miklós Sántha   Pages 1486 - 1494 ( 9 )

Abstract:


Serum lipid levels are closely related to the structure and function of blood vessels. Chronic hyperlipidemia may lead to damage in both the cardio- and the cerebrovascular systems. Vascular dysfunctions, including impairments of the blood-brain barrier, are known to be associated with neurodegenerative diseases. A growing number of evidence suggests that cardiovascular risk factors, such as hyperlipidemia, may increase the likelihood of developing dementia. Due to differences in lipoprotein metabolism, wild-type mice are protected against dietinduced hypercholesterolemia, and their serum lipid profile is different from that observed in humans. Therefore, several transgenic mouse models have been established to study the role of different apolipoproteins and their receptors in lipid metabolism, as well as the complications related to pathological lipoprotein levels. This minireview focused on a transgenic mouse model overexpressing an apolipoprotein, the human ApoB-100. We discussed literature data and current advancements on the understanding of ApoB-100 induced cardio- and cerebrovascular lesions in order to demonstrate the involvement of this type of apolipoprotein in a wide range of pathologies, and a link between hyperlipidemia and neurodegeneration.

Keywords:

ApoB-100 lipoprotein, hyperlipidemia, atherosclerosis, blood-brain barrier (BBB), endothelial dysfunction, cerebrovascular disease, neurodegeneration, dementia, transgenic mice.

Affiliation:

Institute of Biochemistry, Biological Research Centre, Sezeged, Institute of Biochemistry, Biological Research Centre, Sezeged, Institute of Biophysics, Biological Research Centre, H-6726 Szeged, Temesvári krt. 62., Institute of Biochemistry, Biological Research Centre, Sezeged



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