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      Heart failure and Alzheimer′s disease

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          Abstract

          It has recently been proposed that heart failure is a risk factor for Alzheimer′s disease. Decreased cerebral blood flow and neurohormonal activation due to heart failure may contribute to the dysfunction of the neurovascular unit and cause an energy crisis in neurons. This leads to the impaired clearance of amyloid beta and hyperphosphorylation of tau protein, resulting in the formation of amyloid beta plaques and neurofibrillary tangles. In this article, we will summarize the current understanding of the relationship between heart failure and Alzheimer′s disease based on epidemiological studies, brain imaging research, pathological findings and the use of animal models. The importance of atherosclerosis, myocardial infarction, atrial fibrillation, blood pressure and valve disease as well as the effect of relevant medications will be discussed.

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          Most cited references 192

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          Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study.

          Disordered breathing during sleep is associated with acute, unfavorable effects on cardiovascular physiology, but few studies have examined its postulated association with cardiovascular disease (CVD). We examined the cross-sectional association between sleep- disordered breathing and self-reported CVD in 6,424 free-living individuals who underwent overnight, unattended polysomnography at home. Sleep-disordered breathing was quantified by the apnea-hypopnea index (AHI)-the average number of apneas and hypopneas per hour of sleep. Mild to moderate disordered breathing during sleep was highly prevalent in the sample (median AHI: 4.4; interquartile range: 1.3 to 11.0). A total of 1,023 participants (16%) reported at least one manifestation of CVD (myocardial infarction, angina, coronary revascularization procedure, heart failure, or stroke). The multivariable-adjusted relative odds (95% CI) of prevalent CVD for the second, third, and fourth quartiles of the AHI (versus the first) were 0.98 (0.77-1.24), 1.28 (1.02-1.61), and 1.42 (1.13-1.78), respectively. Sleep-disordered breathing was associated more strongly with self-reported heart failure and stroke than with self-reported coronary heart disease: the relative odds (95% CI) of heart failure, stroke, and coronary heart disease (upper versus lower AHI quartile) were 2.38 (1.22-4.62), 1.58 (1.02- 2.46), and 1.27 (0.99-1.62), respectively. These findings are compatible with modest to moderate effects of sleep-disordered breathing on heterogeneous manifestations of CVD within a range of AHI values that are considered normal or only mildly elevated.
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            Heart failure.

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              Neurovascular mechanisms and blood-brain barrier disorder in Alzheimer's disease.

              Vascular dysfunction has a critical role in Alzheimer's disease (AD). Recent data from brain imaging studies in humans and animal models suggest that cerebrovascular dysfunction may precede cognitive decline and onset of neurodegenerative changes in AD and AD models. Cerebral hypoperfusion and impaired amyloid beta-peptide (Abeta) clearance across the blood-brain barrier (BBB) may contribute to the onset and progression of dementia AD type. Decreased cerebral blood flow (CBF) negatively affects the synthesis of proteins required for memory and learning, and may eventually lead to neuritic injury and neuronal death. Impaired clearance of Abeta from the brain by the cells of the neurovascular unit may lead to its accumulation on blood vessels and in brain parenchyma. The accumulation of Abeta on the cerebral blood vessels, known as cerebral amyloid angiopathy (CAA), is associated with cognitive decline and is one of the hallmarks of AD pathology. CAA can severely disrupt the integrity of the blood vessel wall resulting in micro or macro intracerebral bleedings that exacerbates neurodegenerative process and inflammatory response and may lead to hemorrhagic stroke, respectively. Here, we review the role of the neurovascular unit and molecular mechanisms in vascular cells behind AD and CAA pathogenesis. First, we discuss apparent vascular changes, including the cerebral hypoperfusion and vascular degeneration that contribute to different stages of the disease process in AD individuals. We next discuss the role of the low-density lipoprotein receptor related protein-1 (LRP), a key Abeta clearance receptor at the BBB and along the cerebrovascular system, whose expression is suppressed early in AD. We also discuss how brain-derived apolipoprotein E isoforms may influence Abeta clearance across the BBB. We then review the role of two interacting transcription factors, myocardin and serum response factor, in cerebral vascular cells in controlling CBF responses and LRP-mediated Abeta clearance. Finally, we discuss the role of microglia and perivascular macrophages in Abeta clearance from the brain. The data reviewed here support an essential role of neurovascular and BBB mechanisms in contributing to both, onset and progression of AD.
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                Author and article information

                Journal
                J Intern Med
                J. Intern. Med
                joim
                Journal of Internal Medicine
                BlackWell Publishing Ltd (Oxford, UK )
                0954-6820
                1365-2796
                April 2015
                01 August 2014
                : 277
                : 4
                : 406-425
                Affiliations
                [1 ]Division for Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet Huddinge, Sweden
                [2 ]International Clinical Research Center and St. Anne's University Hospital Brno, Czech Republic
                [3 ]Department of Geriatric Medicine, Karolinska University Hospital Stockholm, Sweden
                [4 ]Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet Stockholm, Sweden
                [5 ]Department of Cardiology, Karolinska University Hospital Stockholm, Sweden
                [6 ]Unit of Cardiology, Department of Medicine, Karolinska Institutet Stockholm, Sweden
                [7 ]Department of Medicine, Center for Molecular Medicine, Karolinska Institutet Stockholm, Sweden
                Author notes
                Correspondence: Pavla Cermakova, MD and Prof. Bengt Winblad, MD, PhD, Division for Neurogeriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Blickagången 6, Novum, 141 57 Huddinge, Sweden., (fax: +46 (8)58585470; e-mail: Pavla.Cermakova@ 123456ki.se )., (fax: +46 70-632 67 71; e-mail: bengt.winblad@ 123456ki.se ).

                Click here to view the article Editorial Comment by A. E. Roher

                Article
                10.1111/joim.12287
                4409079
                25041352
                ece4a908-e961-40c6-93cb-caac3b2ee31e
                © 2014 The Authors. Journal of Internal Medicine published by John Wiley & Sons Ltd on behalf of The Association for the Publication of the Journal of Internal Medicine.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                Categories
                Review Articles

                Internal medicine

                alzheimer′s disease, dementia, heart failure, neurocardiology, neurovascular unit

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