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Increases in the Risk of Cognitive Impairment and Alterations of Cerebral β-amyloid Metabolism in Mouse Model of Heart Failure

Epidemiological and clinico-pathological studies indicate a causal relationship between heart disease and Alzheimer’s disease (AD). To learn whether heart disease causes an onset of AD, mice with myocardial infarction (MI) and congestive heart failure (HF) were used to test neuropsychiatric and cogn...

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Autores principales: Hong, Xiaoqi, Bu, Liping, Wang, Yi, Xu, Jing, Wu, Jian, Huang, Yufang, Liu, Jie, Suo, Haiyun, Yang, Lumeng, Shi, Yuncen, Lou, Yi, Sun, Zhengliang, Zhu, Guoqi, Behnisch, Thomas, Yu, Mei, Jia, Jianguo, Hai, Wangxi, Meng, Hongping, Liang, Sheng, Huang, Fang, Zou, Yunzeng, Ge, Junbo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667825/
https://www.ncbi.nlm.nih.gov/pubmed/23737953
http://dx.doi.org/10.1371/journal.pone.0063829
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author Hong, Xiaoqi
Bu, Liping
Wang, Yi
Xu, Jing
Wu, Jian
Huang, Yufang
Liu, Jie
Suo, Haiyun
Yang, Lumeng
Shi, Yuncen
Lou, Yi
Sun, Zhengliang
Zhu, Guoqi
Behnisch, Thomas
Yu, Mei
Jia, Jianguo
Hai, Wangxi
Meng, Hongping
Liang, Sheng
Huang, Fang
Zou, Yunzeng
Ge, Junbo
author_facet Hong, Xiaoqi
Bu, Liping
Wang, Yi
Xu, Jing
Wu, Jian
Huang, Yufang
Liu, Jie
Suo, Haiyun
Yang, Lumeng
Shi, Yuncen
Lou, Yi
Sun, Zhengliang
Zhu, Guoqi
Behnisch, Thomas
Yu, Mei
Jia, Jianguo
Hai, Wangxi
Meng, Hongping
Liang, Sheng
Huang, Fang
Zou, Yunzeng
Ge, Junbo
author_sort Hong, Xiaoqi
collection PubMed
description Epidemiological and clinico-pathological studies indicate a causal relationship between heart disease and Alzheimer’s disease (AD). To learn whether heart disease causes an onset of AD, mice with myocardial infarction (MI) and congestive heart failure (HF) were used to test neuropsychiatric and cognitive behaviors as well as for measurements of AD related protein markers. To this end, adult mice were subjected to ligation of left anterior descending artery (LAD) and about two weeks later high-frequency echocardiography was performed to exam the resulting cardiac structure and function. Three months after successful induction of chronic heart failure (CHF) these mice showed an impairment of learning in the Morris Water Maze task. In addition, the expression of selected molecules, which are involved in β-amyloid metabolism, apoptosis and inflammation on the level of gene transcription and translation, was altered in CHF mice. Our findings provide a plausible explanation that CHF increases the risk of cognitive impairments and alters cerebral β-amyloid metabolism. In addition, our data indicate that the cerebral compensatory mechanisms in response to CHF are brain area and gender specific.
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spelling pubmed-36678252013-06-04 Increases in the Risk of Cognitive Impairment and Alterations of Cerebral β-amyloid Metabolism in Mouse Model of Heart Failure Hong, Xiaoqi Bu, Liping Wang, Yi Xu, Jing Wu, Jian Huang, Yufang Liu, Jie Suo, Haiyun Yang, Lumeng Shi, Yuncen Lou, Yi Sun, Zhengliang Zhu, Guoqi Behnisch, Thomas Yu, Mei Jia, Jianguo Hai, Wangxi Meng, Hongping Liang, Sheng Huang, Fang Zou, Yunzeng Ge, Junbo PLoS One Research Article Epidemiological and clinico-pathological studies indicate a causal relationship between heart disease and Alzheimer’s disease (AD). To learn whether heart disease causes an onset of AD, mice with myocardial infarction (MI) and congestive heart failure (HF) were used to test neuropsychiatric and cognitive behaviors as well as for measurements of AD related protein markers. To this end, adult mice were subjected to ligation of left anterior descending artery (LAD) and about two weeks later high-frequency echocardiography was performed to exam the resulting cardiac structure and function. Three months after successful induction of chronic heart failure (CHF) these mice showed an impairment of learning in the Morris Water Maze task. In addition, the expression of selected molecules, which are involved in β-amyloid metabolism, apoptosis and inflammation on the level of gene transcription and translation, was altered in CHF mice. Our findings provide a plausible explanation that CHF increases the risk of cognitive impairments and alters cerebral β-amyloid metabolism. In addition, our data indicate that the cerebral compensatory mechanisms in response to CHF are brain area and gender specific. Public Library of Science 2013-05-30 /pmc/articles/PMC3667825/ /pubmed/23737953 http://dx.doi.org/10.1371/journal.pone.0063829 Text en © 2013 Hong et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Hong, Xiaoqi
Bu, Liping
Wang, Yi
Xu, Jing
Wu, Jian
Huang, Yufang
Liu, Jie
Suo, Haiyun
Yang, Lumeng
Shi, Yuncen
Lou, Yi
Sun, Zhengliang
Zhu, Guoqi
Behnisch, Thomas
Yu, Mei
Jia, Jianguo
Hai, Wangxi
Meng, Hongping
Liang, Sheng
Huang, Fang
Zou, Yunzeng
Ge, Junbo
Increases in the Risk of Cognitive Impairment and Alterations of Cerebral β-amyloid Metabolism in Mouse Model of Heart Failure
title Increases in the Risk of Cognitive Impairment and Alterations of Cerebral β-amyloid Metabolism in Mouse Model of Heart Failure
title_full Increases in the Risk of Cognitive Impairment and Alterations of Cerebral β-amyloid Metabolism in Mouse Model of Heart Failure
title_fullStr Increases in the Risk of Cognitive Impairment and Alterations of Cerebral β-amyloid Metabolism in Mouse Model of Heart Failure
title_full_unstemmed Increases in the Risk of Cognitive Impairment and Alterations of Cerebral β-amyloid Metabolism in Mouse Model of Heart Failure
title_short Increases in the Risk of Cognitive Impairment and Alterations of Cerebral β-amyloid Metabolism in Mouse Model of Heart Failure
title_sort increases in the risk of cognitive impairment and alterations of cerebral β-amyloid metabolism in mouse model of heart failure
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3667825/
https://www.ncbi.nlm.nih.gov/pubmed/23737953
http://dx.doi.org/10.1371/journal.pone.0063829
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