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Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators
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Zeitschriftentitel: | Journal of Neurochemistry |
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Personen und Körperschaften: | |
In: | Journal of Neurochemistry, 115, 2010, 3, S. 551-562 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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Schlagwörter: |
author_facet |
Bhat, Narayan R. Bhat, Narayan R. |
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author |
Bhat, Narayan R. |
spellingShingle |
Bhat, Narayan R. Journal of Neurochemistry Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators Cellular and Molecular Neuroscience Biochemistry |
author_sort |
bhat, narayan r. |
spelling |
Bhat, Narayan R. 0022-3042 1471-4159 Wiley Cellular and Molecular Neuroscience Biochemistry http://dx.doi.org/10.1111/j.1471-4159.2010.06978.x <jats:sec><jats:label /><jats:p> <jats:italic>J. Neurochem.</jats:italic> (2010) <jats:bold>115</jats:bold>, 551–562.</jats:p></jats:sec><jats:sec><jats:title>Abstract</jats:title><jats:p>There is increasing evidence that the incidence of Alzheimer’s disease (AD) is significantly influenced by cardiovascular risk factors in association with a cluster of metabolic diseases including diabetes and atherosclerosis. The shared risk is also reflected in the dietary and lifestyle links to both metabolic disorders and AD‐type cognitive dysfunction. Recent studies with genetic and diet‐induced animal models have begun to illuminate convergent mechanisms and mediators between these two categories of disease conditions with distinct tissue‐specific pathologies. Although it is clear that peripheral inflammation and insulin resistance are central to the pathogenesis of the disorders of metabolic syndrome, it seems that the same mechanisms are also in play across the blood–brain barrier that lead to AD‐like molecular and cognitive changes. This review highlights these convergent mechanisms and discusses the role of cerebrovascular dysfunction as a conduit to brain emergence of these pathogenic processes that might also represent future therapeutic targets in AD in common with metabolic disorders.</jats:p></jats:sec> Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators Journal of Neurochemistry |
doi_str_mv |
10.1111/j.1471-4159.2010.06978.x |
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Online Free |
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Biologie Psychologie Chemie und Pharmazie |
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Wiley, 2010 |
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Wiley, 2010 |
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2010 |
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Wiley |
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Journal of Neurochemistry |
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title |
Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_unstemmed |
Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_full |
Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_fullStr |
Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_full_unstemmed |
Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_short |
Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_sort |
linking cardiometabolic disorders to sporadic alzheimer’s disease: a perspective on potential mechanisms and mediators |
topic |
Cellular and Molecular Neuroscience Biochemistry |
url |
http://dx.doi.org/10.1111/j.1471-4159.2010.06978.x |
publishDate |
2010 |
physical |
551-562 |
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<jats:sec><jats:label /><jats:p> <jats:italic>J. Neurochem.</jats:italic> (2010) <jats:bold>115</jats:bold>, 551–562.</jats:p></jats:sec><jats:sec><jats:title>Abstract</jats:title><jats:p>There is increasing evidence that the incidence of Alzheimer’s disease (AD) is significantly influenced by cardiovascular risk factors in association with a cluster of metabolic diseases including diabetes and atherosclerosis. The shared risk is also reflected in the dietary and lifestyle links to both metabolic disorders and AD‐type cognitive dysfunction. Recent studies with genetic and diet‐induced animal models have begun to illuminate convergent mechanisms and mediators between these two categories of disease conditions with distinct tissue‐specific pathologies. Although it is clear that peripheral inflammation and insulin resistance are central to the pathogenesis of the disorders of metabolic syndrome, it seems that the same mechanisms are also in play across the blood–brain barrier that lead to AD‐like molecular and cognitive changes. This review highlights these convergent mechanisms and discusses the role of cerebrovascular dysfunction as a conduit to brain emergence of these pathogenic processes that might also represent future therapeutic targets in AD in common with metabolic disorders.</jats:p></jats:sec> |
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description | <jats:sec><jats:label /><jats:p> <jats:italic>J. Neurochem.</jats:italic> (2010) <jats:bold>115</jats:bold>, 551–562.</jats:p></jats:sec><jats:sec><jats:title>Abstract</jats:title><jats:p>There is increasing evidence that the incidence of Alzheimer’s disease (AD) is significantly influenced by cardiovascular risk factors in association with a cluster of metabolic diseases including diabetes and atherosclerosis. The shared risk is also reflected in the dietary and lifestyle links to both metabolic disorders and AD‐type cognitive dysfunction. Recent studies with genetic and diet‐induced animal models have begun to illuminate convergent mechanisms and mediators between these two categories of disease conditions with distinct tissue‐specific pathologies. Although it is clear that peripheral inflammation and insulin resistance are central to the pathogenesis of the disorders of metabolic syndrome, it seems that the same mechanisms are also in play across the blood–brain barrier that lead to AD‐like molecular and cognitive changes. This review highlights these convergent mechanisms and discusses the role of cerebrovascular dysfunction as a conduit to brain emergence of these pathogenic processes that might also represent future therapeutic targets in AD in common with metabolic disorders.</jats:p></jats:sec> |
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spelling | Bhat, Narayan R. 0022-3042 1471-4159 Wiley Cellular and Molecular Neuroscience Biochemistry http://dx.doi.org/10.1111/j.1471-4159.2010.06978.x <jats:sec><jats:label /><jats:p> <jats:italic>J. Neurochem.</jats:italic> (2010) <jats:bold>115</jats:bold>, 551–562.</jats:p></jats:sec><jats:sec><jats:title>Abstract</jats:title><jats:p>There is increasing evidence that the incidence of Alzheimer’s disease (AD) is significantly influenced by cardiovascular risk factors in association with a cluster of metabolic diseases including diabetes and atherosclerosis. The shared risk is also reflected in the dietary and lifestyle links to both metabolic disorders and AD‐type cognitive dysfunction. Recent studies with genetic and diet‐induced animal models have begun to illuminate convergent mechanisms and mediators between these two categories of disease conditions with distinct tissue‐specific pathologies. Although it is clear that peripheral inflammation and insulin resistance are central to the pathogenesis of the disorders of metabolic syndrome, it seems that the same mechanisms are also in play across the blood–brain barrier that lead to AD‐like molecular and cognitive changes. This review highlights these convergent mechanisms and discusses the role of cerebrovascular dysfunction as a conduit to brain emergence of these pathogenic processes that might also represent future therapeutic targets in AD in common with metabolic disorders.</jats:p></jats:sec> Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators Journal of Neurochemistry |
spellingShingle | Bhat, Narayan R., Journal of Neurochemistry, Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators, Cellular and Molecular Neuroscience, Biochemistry |
title | Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_full | Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_fullStr | Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_full_unstemmed | Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_short | Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_sort | linking cardiometabolic disorders to sporadic alzheimer’s disease: a perspective on potential mechanisms and mediators |
title_unstemmed | Linking cardiometabolic disorders to sporadic Alzheimer’s disease: a perspective on potential mechanisms and mediators |
topic | Cellular and Molecular Neuroscience, Biochemistry |
url | http://dx.doi.org/10.1111/j.1471-4159.2010.06978.x |