Increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.

<h4>Aims</h4>ApoB-100 is the major protein component of cholesterol- and triglyceride-rich LDL and VLDL lipoproteins in the serum. Previously, we generated and partially described transgenic mice overexpressing the human ApoB-100 protein. Here, we further characterize this transgenic str...

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Autores principales:	Nikolett Lénárt, Viktor Szegedi, Gábor Juhász, Aniko Kasztner, János Horváth, Erika Bereczki, Melinda E Tóth, Botond Penke, Miklós Sántha
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/50388ac2af4d4398862f55cad7d2d37b
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spelling	oai:doaj.org-article:50388ac2af4d4398862f55cad7d2d37b2021-11-18T07:04:16ZIncreased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.1932-620310.1371/journal.pone.0046007https://doaj.org/article/50388ac2af4d4398862f55cad7d2d37b2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23029362/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Aims</h4>ApoB-100 is the major protein component of cholesterol- and triglyceride-rich LDL and VLDL lipoproteins in the serum. Previously, we generated and partially described transgenic mice overexpressing the human ApoB-100 protein. Here, we further characterize this transgenic strain in order to reveal a possible link between hypeprlipidemia and neurodegeneration.<h4>Methods and results</h4>We analyzed the serum and cerebral lipid profiles, tau phosphorylation patterns, amyloid plaque-formation, neuronal apoptosis and synaptic plasticity of young (3 month old), adult (6 month old) and aging (10-11 month old) transgenic mice. We show that ApoB-100 transgenic animals present i) elevated serum and cerebral levels of triglycerides and ApoB-100, ii) increased cerebral tau phosphorylation at phosphosites Ser(199), Ser(199/202), Ser(396) and Ser(404). Furthermore, we demonstrate, that tau hyperphosphorylation is accompanied by impaired presynaptic function, long-term potentiation and widespread hippocampal neuronal apoptosis.<h4>Conclusions</h4>The results presented here indicate that elevated ApoB-100 level and the consequent chronic hypertriglyceridemia may lead to impaired neuronal function and neurodegeneration, possibly via hyperphosphorylation of tau protein. On account of their specific phenotype, ApoB-100 transgenic mice may be considered a versatile model of hyperlipidemia-induced age-related neurodegeneration.Nikolett LénártViktor SzegediGábor JuhászAniko KasztnerJános HorváthErika BereczkiMelinda E TóthBotond PenkeMiklós SánthaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e46007 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Nikolett Lénárt Viktor Szegedi Gábor Juhász Aniko Kasztner János Horváth Erika Bereczki Melinda E Tóth Botond Penke Miklós Sántha Increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.
description	<h4>Aims</h4>ApoB-100 is the major protein component of cholesterol- and triglyceride-rich LDL and VLDL lipoproteins in the serum. Previously, we generated and partially described transgenic mice overexpressing the human ApoB-100 protein. Here, we further characterize this transgenic strain in order to reveal a possible link between hypeprlipidemia and neurodegeneration.<h4>Methods and results</h4>We analyzed the serum and cerebral lipid profiles, tau phosphorylation patterns, amyloid plaque-formation, neuronal apoptosis and synaptic plasticity of young (3 month old), adult (6 month old) and aging (10-11 month old) transgenic mice. We show that ApoB-100 transgenic animals present i) elevated serum and cerebral levels of triglycerides and ApoB-100, ii) increased cerebral tau phosphorylation at phosphosites Ser(199), Ser(199/202), Ser(396) and Ser(404). Furthermore, we demonstrate, that tau hyperphosphorylation is accompanied by impaired presynaptic function, long-term potentiation and widespread hippocampal neuronal apoptosis.<h4>Conclusions</h4>The results presented here indicate that elevated ApoB-100 level and the consequent chronic hypertriglyceridemia may lead to impaired neuronal function and neurodegeneration, possibly via hyperphosphorylation of tau protein. On account of their specific phenotype, ApoB-100 transgenic mice may be considered a versatile model of hyperlipidemia-induced age-related neurodegeneration.
format	article
author	Nikolett Lénárt Viktor Szegedi Gábor Juhász Aniko Kasztner János Horváth Erika Bereczki Melinda E Tóth Botond Penke Miklós Sántha
author_facet	Nikolett Lénárt Viktor Szegedi Gábor Juhász Aniko Kasztner János Horváth Erika Bereczki Melinda E Tóth Botond Penke Miklós Sántha
author_sort	Nikolett Lénárt
title	Increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.
title_short	Increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.
title_full	Increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.
title_fullStr	Increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.
title_full_unstemmed	Increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.
title_sort	increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic apob-100 transgenic mice.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/50388ac2af4d4398862f55cad7d2d37b
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Increased tau phosphorylation and impaired presynaptic function in hypertriglyceridemic ApoB-100 transgenic mice.

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