Cardiovascular psychiatry and neurology最新文献

{"title":"Role of Hypertension in Aggravating Abeta Neuropathology of AD Type and Tau-Mediated Motor Impairment.","authors":"C Díaz-Ruiz,&nbsp;J Wang,&nbsp;H Ksiezak-Reding,&nbsp;L Ho,&nbsp;X Qian,&nbsp;N Humala,&nbsp;S Thomas,&nbsp;P Martínez-Martín,&nbsp;G M Pasinetti","doi":"10.1155/2009/107286","DOIUrl":"https://doi.org/10.1155/2009/107286","url":null,"abstract":"<p><p>Epidemiological evidence suggests that hypertension may accelerate the onset and progression of Alzheimer's disease (AD). In this study, we explored the role of hypertension in the neurodegenerative changes associated with Abeta and tau aggregation. We induced hypertension in APP(swe) Tg2576 and P301L-tauTg mouse models. In Tg2576 mice, experimental hypertension was associated with a significant increase of the accumulation of Amyloid-beta (Abeta) peptides in brain tissue and a significant reduction of Abeta peptides in serum (P < .05). These results indicate that hypertension may promote AD-type Abeta neuropathology in Tg2576. In P301L-tauTg mice we found that the presence of hypertension was significantly associated with aggravated motor function assessed by hindlimb extension test (P = .01). These results suggest that hypertension may play a role in accelerating the progression of motor dysfunction associated with tau-related alterations. Our studies suggest that the management of blood pressure (BP) may alleviate AD-type Abeta neuropathology and neurological disorders associated with abnormal tau metabolism.</p>","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"107286"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/107286","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28527101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The 5-lipoxygenase as a common pathway for pathological brain and vascular aging.","authors":"Jin Chu,&nbsp;Domenico Praticò","doi":"10.1155/2009/174657","DOIUrl":"https://doi.org/10.1155/2009/174657","url":null,"abstract":"<p><p>Epidemiological studies indicate age as a strong risk factor for developing cardiovascular and neurodegenerative diseases. During the aging process, changes in the expression of particular genes can influence the susceptibility to these diseases. 5-Lipoxygenase (5-LO) by oxidizing fatty acids forms leukotrienes, potent mediators of oxidative and inflammatory reactions, two key pathogenic events in both clinical settings. This enzyme is widely distributed in the cardiovascular as well as in the central nervous system, where its expression levels increase with age, suggesting that it may be involved in their diseases of aging. The central theme of this article is that during aging, 5-LO acts as biologic link between different stressors and the development of cardiovascular and neurodegenerative diseases. We hypothesize that the age-dependent upregulation of 5-LO represents a \"priming\" factor in the vasculature as well as in the brain, where a subsequent exposure to triggering stimuli (i.e., infections) leads to an abnormal chronic inflammatory reaction, and ultimately results in increased organ vulnerability and functional deficits.</p>","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"174657"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/174657","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28527102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The heart-brain connection begets cardiovascular psychiatry and neurology.","authors":"Hari Manev","doi":"10.1155/2009/546737","DOIUrl":"https://doi.org/10.1155/2009/546737","url":null,"abstract":"In many Asian languages, the same ancient letter/symbol is used for heart and mind. For the last couple of millennia, physicians and scientists across different civilizations have posited close links between the brain and heart, even arguing that the site of intelligence and emotions is in one of these two organs. Through an integrative empirical approach in modern biology/physiology and behavioral sciences, much has since been learned to confirm the anatomical and functional links between the brain and the heart. Arguably, the ultimate applicability of this knowledge will advance our health and improve disease treatment. \u0000 \u0000Modern medicine is characterized by a high degree of specialization, and the heart-brain connection is typically considered from the point of view of a particular medical specialty. Hence, focusing on the brain, for example, in neurology, cardiovascular involvement is critical in certain pathologies such as stroke and vascular dementia. In cardiology, on the other hand, the influence of the brain becomes clearly apparent in “the broken heart syndrome” (also known as acute stress cardiomyopathy). However, recent epidemiological studies point to new associations that typically present as co-occurring pathologies of both the brain and the heart. A case in point is the association between depression and coronary heart disease. Such co-occurrences have stimulated research into possible novel mechanisms that could be targeted to treat these complex cardiovascular/brain disorders. \u0000 \u0000At least three scenarios could be at play in these illnesses: (i) the primary pathological mechanism in the nervous system triggers a cardiovascular pathology by disrupting physiological links between the two systems (hence, the term “psychogenic”cardiovascular disease), (ii) the primary pathological mechanism in the cardiovascular system triggers a nervous system dysfunction (e.g., atherosclerosis leading to ischemic conditions causes subsequent cognitive impairment), and (iii) the primary pathology is in a biological mechanism that is normally operative in both the nervous and the cardiovascular systems, thus causing the co-occurrence of pathologies (i.e., the co-occurring pathologies share a pathobiological mechanism but do not necessarily cause each other). \u0000 \u0000To be successful, research in co-occurring cardiovascular and brain disorders needs contributions from multiple medical specialties, including psychiatry, neurology, medicine, and cardiology. It should encompass clinical and basic research as well as the development of therapeutic approaches. The purpose of Cardiovascular Psychiatry and Neurology is to provide a platform for the latest research and for timely and expert reviews and comments in the emerging field of cardiovascular psychiatry and neurology. Although the term cardiovascular psychiatry and neurology is introduced here for the first time, retrieving publications from PubMed using either cardiovascular psychiatry or cardiovascular n","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"546737"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/546737","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28609841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heart and brain tissue banks for research on co-occurring cardiovascular and neurological/psychiatric disorders.","authors":"Milos D Ikonomovic","doi":"10.1155/2009/427840","DOIUrl":"https://doi.org/10.1155/2009/427840","url":null,"abstract":"<p><p>Epidemiological studies point to a strong and possibly causal association of psychiatric and neurological disorders with cardiovascular disease (CVD). Mechanistic links between these co-occurring illnesses are not well understood. Better insight into their relationship could help identify novel diagnostic markers and therapeutic targets. For successful translation of basic biomedical research into clinical practice, analyses of postmortem human tissues are essential. However, current tissue banks dedicated to psychiatric and neurological research collect only brain tissue samples deemed most important to the institution's participating investigators. While this practice is often dictated by budget constraints, restricted tissue storage space and other practical reasons, it limits the ability of the biological research community to access and study multiple organ systems relevant to cardiovascular and neuronal systems dysfunction. This problem is worsened when clinical records pertaining to coexistent systemic pathology are not available. To promote further understanding of co-occurring CVD and psychiatric/neurological disorders, efforts should be made to support tissue banks that harvest heart, coronary arteries, and aorta samples as well as brain tissue, from the same subjects.</p>","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"427840"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/427840","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28609776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Matrix Metalloproteinase-9 (MMP9)-A Mediating Enzyme in Cardiovascular Disease, Cancer, and Neuropsychiatric Disorders.","authors":"Janusz K Rybakowski","doi":"10.1155/2009/904836","DOIUrl":"https://doi.org/10.1155/2009/904836","url":null,"abstract":"<p><p>Matrix metalloproteinase-9 (MMP9) has been implicated in numerous somatic illnesses, including cardiovascular disorders and cancer. Recently, MMP9 has been shown to be increasingly important in several aspects of central nervous system activity. Furthermore, a pathogenic role for this enzyme has been suggested in such neuropsychiatric disorders as schizophrenia, bipolar illness, and multiple sclerosis. In this paper, the results of biochemical and molecular-genetic studies on MMP9 that have been performed in these pathological conditions will be summarized. Furthermore, I hypothesize that the MMP9 gene, as shown by functional -1562 C/T polymorphism studies, may be mediating the relationship of neuropsychiatric illnesses (schizophrenia, bipolar mood disorder, multiple sclerosis) that are comorbid with cardiovascular disease and cancer.</p>","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"904836"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/904836","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28618362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Membrane omega-3 Fatty Acid deficiency as a preventable risk factor for comorbid coronary heart disease in major depressive disorder.","authors":"Robert K McNamara","doi":"10.1155/2009/362795","DOIUrl":"https://doi.org/10.1155/2009/362795","url":null,"abstract":"<p><p>Major depression disorder (MDD) significantly increases the risk for coronary heart disease (CHD) which is a leading cause of mortality in patients with MDD. Moreover, depression is frequently observed in a subset of patients following acute coronary syndrome (ACS) and increases risk for mortality. Here evidence implicating omega-3 (n-3) fatty acid deficiency in the pathoaetiology of CHD and MDD is reviewed, and the hypothesis that n-3 fatty acid deficiency is a preventable risk factor for CHD comorbidity in MDD patients is evaluated. This hypothesis is supported by cross-national and cross-sectional epidemiological surveys finding an inverse correlation between n-3 fatty acid status and prevalence rates of both CHD and MDD, prospective studies finding that lower dietary or membrane EPA+DHA levels increase risk for both MDD and CHD, case-control studies finding that the n-3 fatty acid status of MDD patients places them at high risk for emergent CHD morbidity and mortality, meta-analyses of controlled n-3 fatty acid intervention studies finding significant advantage over placebo for reducing depression symptom severity in MDD patients, and for secondary prevention of cardiac events in CHD patients, findings that n-3 fatty acid status is inversely correlated with other documented CHD risk factors, and patients diagnosed with MDD after ACS exhibit significantly lower n-3 fatty acid status compared with nondepressed ACS patients. This body of evidence provides strong support for future studies to evaluate the effects of increasing dietary n-3 fatty acid status on CHD comorbidity and mortality in MDD patients.</p>","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"362795"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/362795","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28527055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serotonin 5-HT(2A) Receptor Function as a Contributing Factor to Both Neuropsychiatric and Cardiovascular Diseases.","authors":"Charles D Nichols","doi":"10.1155/2009/475108","DOIUrl":"https://doi.org/10.1155/2009/475108","url":null,"abstract":"<p><p>There are high levels of comorbidity between neuropsychiatric and cardiovascular disorders. A key molecule central to both cognitive and cardiovascular function is the molecule serotonin. In the brain, serotonin modulates neuronal activity and is actively involved in mediating many cognitive functions and behaviors. In the periphery, serotonin is involved in vasoconstriction, inflammation, and cell growth, among other processes. It is hypothesized that one component of the serotonin system, the 5-HT(2A) receptor, is a common and contributing factor underlying aspects of the comorbidity between neuropsychiatric and cardiovascular disorders. Within the brain this receptor participates in processes such as cognition and working memory, been implicated in effective disorders such as schizophrenia, and mediate the primary effects of hallucinogenic drugs. In the periphery, 5-HT(2A) receptors have been linked to vasoconstriction and hypertension, and to inflammatory processes that can lead to atherosclerosis.</p>","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"475108"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/475108","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28610277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypotheses on mechanisms linking cardiovascular and psychiatric/neurological disorders.","authors":"Hari Manev","doi":"10.1155/2009/197132","DOIUrl":"https://doi.org/10.1155/2009/197132","url":null,"abstract":"This special issue of Cardiovascular Psychiatry and Neurology marks its first year since we launched the open access journal dedicated to publishing original preclinical/basic and research on biological mechanisms of and treatments for co-occurring cardiovascular disorders and disorders of the central nervous system (CNS). As suggested earlier (by the paper entitled “The heart-brain connection begets cardiovascular psychiatry and neurology” by Hari Manev), at least three scenarios could be at play in these disorders: (1) the primary pathological mechanism in the cardiovascular system triggers a nervous system dysfunction, (2) the primary pathological mechanism in the nervous system triggers a cardiovascular pathology by disrupting the physiological links between the two systems, and (3) the primary pathology is in a biological mechanism that is normally operative in both the nervous and the cardiovascular systems, thus causing the cooccurrence of pathologies, that is, the cooccurring pathologies share a pathobiological mechanism but do not necessarily cause each other. The ongoing research explores the validity of these conceptual scenarios. \u0000 \u0000Whereas the evidence for the association of cardiovascular and CNS disorders derives primarily from epidemiological studies, direct evidence and experimental data are just beginning to emerge to support this notion. Difficulties in directly demonstrating and explaining the cooccurrence of cardiovascular and CNS disorders lie in part in the limitations of their respective animal models (in particular animal models of psychiatric disorders) and in part in conceptual uncertainties regarding the mechanisms linking heart-brain pathologies that hamper respective clinical research. Historically, bold hypotheses along with serendipitous observations have been instrumental in breakthrough discoveries. \u0000 \u0000This collection of hypotheses on mechanisms linking cardiovascular and psychiatric/neurological disorders has been assembled with the goal of stimulating discussions in this field of bioscience and medicine. The postulated mechanisms range from molecular targets and pathways (the papers by Sebastien S. Hebert entitled “Putative role of microRNA regulated pathways in comorbid neurological and cardiovascular disorders”, by David P. Gavin and Rajiv P. Sharma entitled “Chromatin from peripheral blood mononuclear cells as biomarkers for epigenetic abnormalities in schizophrenia”, by Neil R. Smalheiser entitled “Do neural cells communicate with endothelial cells via secretory exosomes and microvesicles?” by Stephen D. Skaper and Pietro Giusti entitled “P2X7 receptors as a transducer in the cooccurrence of neurological/psychiatric and cardiovascular disorders: A hypothesis”, by Charles D Nichols entitled “Serotonin 5-HT2A receptor function as a contributing factor to both neuropsychiatric and cardiovascular diseases” by Hu Chen entitled “Possible role of platelet GluR1 receptors in comorbid depression and cardiovascular d","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"197132"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/197132","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28609771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Possible Role of Platelet GluR1 Receptors in Comorbid Depression and Cardiovascular Disease.","authors":"Hu Chen","doi":"10.1155/2009/424728","DOIUrl":"https://doi.org/10.1155/2009/424728","url":null,"abstract":"<p><p>The exact nature of the comorbidity between cardiovascular disease (CVD) and major depressive disorder (MDD) is poorly understood. The proposed mechanisms include various biochemical and molecular pathways as well as health behaviors such as physical inactivity. One possible link between MDD and CVD is increased platelet activity and blood viscosity. Recently, it was discovered that platelets express functional subtype of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, for example, glutamate receptor 1 (GluR1). Here, I propose that this type of AMPA receptor could play a role in comorbid MDD and CVD, and antidepressants may interfere with platelet activation via direct or indirect effects on platelet GluR1 phosphorylation. Testing this hypothesis could provide a novel view on the pathobiological mechanisms of comorbid MDD and CVD. With respect to the recently discovered role of AMPA receptors in regulating platelet activation and thrombosis, it appears that the information about the putative effects of psychoactive AMPA-modifying drugs on platelet AMPA receptors would be critical in evaluating the putative effects of such drugs on CVD.</p>","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"424728"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/424728","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28609775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2X(7) Receptors as a Transducer in the Co-Occurrence of Neurological/Psychiatric and Cardiovascular Disorders: A Hypothesis.","authors":"Stephen D Skaper,&nbsp;Pietro Giusti","doi":"10.1155/2009/545263","DOIUrl":"https://doi.org/10.1155/2009/545263","url":null,"abstract":"<p><p>Background. Over-stimulation of the purinergic P2X(7) receptor may bring about cellular dysfunction and injury in settings of neurodegeneration, chronic inflammation, as well as in psychiatric and cardiovascular diseases. Here we speculate how P2X(7) receptor over-activation may lead to the co-occurrence of neurological and psychiatric disorders with cardiovascular disorders. Presentation. We hypothesize that proinflammatory cytokines, in particular interleukin-1beta, are key players in the pathophysiology of neurological, psychiatric, and cardiovascular diseases. Critically, this premise is based on a role for the P2X(7) receptor in triggering a rise in these cytokines. Given the broad distribution of P2X(7) receptors in nervous, immune, and vascular tissue cells, this receptor is proposed as central in linking the nervous, immune, and cardiovascular systems. Testing. Investigate, retrospectively, whether a bidirectional link can be established between illnesses with a proinflammatory component (e.g., inflammatory and chronic neuropathic pain) and cardiovascular disease, for example, hypertension, and whether patients treated with anti-inflammatory drugs have a lower incidence of disease complications. Positive outcome would indicate a prospective study to evaluate therapeutic efficacy of P2X(7) receptor antagonists. Implications. It should be stressed that sufficient direct evidence does not exist at present supporting our hypothesis. However, a positive outcome would encourage the further development of P2X(7) receptor antagonists and their application to limit the co-occurrence of neurological, psychiatric, and cardiovascular disorders.</p>","PeriodicalId":88441,"journal":{"name":"Cardiovascular psychiatry and neurology","volume":"2009 ","pages":"545263"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2009/545263","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28610278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}