35
views
0
recommends
+1 Recommend
1 collections
    0
    shares

      Neuropsychiatric Disease and Treatment (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on all aspects of neuropsychiatric and neurological disorders. Sign up for email alerts here.

      63,741 Monthly downloads/views I 2.989 Impact Factor I 4.5 CiteScore I 1.09 Source Normalized Impact per Paper (SNIP) I 0.744 Scimago Journal & Country Rank (SJR)

      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Platelet activating factors are associated with depressive symptoms in coronary artery disease patients: a hypothesis-generating study

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Introduction

          Depression is a frequent complication of coronary artery disease (CAD) with an unknown etiology. Platelet activating factor (PAF) lipids, which are associated with CAD, have recently been linked with novel proposed etiopathological mechanisms for depression such as inflammation, oxidative/nitrosative stress, and vascular endothelial dysfunction.

          Methods and results

          This hypothesis-generating study investigated the relationships between various PAF species and depressive symptoms in 26 CAD patients (age: 60.6±9.2 years, 69% male, mean Hamilton Depression Rating Scale [HAM-D] score: 11.8±5.2, HAM-D range: 3–20). Plasma PAF analyses were performed using high performance liquid chromatography electrospray ionization mass spectrometry in precursor ion scan. Significant associations between depressive symptom severity (HAM-D score) and a greater plasma abundance of the PAFs phosphocholine (PC) PC( O-12:0/2:0) ( r=0.49, P=0.01), PC( O-14:1/2:0) ( r=0.43, P=0.03), PC( O-17:3/2:0) ( r=0.44, P=0.04), and PC( O-18:3/2:0) ( r=0.50, P=0.01) were observed. Associations between those PAFs and HAM-D score persisted after adjusting for age and sex.

          Conclusion

          These preliminary findings support the exploration of the PAF lipidome for depressive symptom biomarkers in CAD patients. Patients were recruited as part of the following clinical trial: NCT00981383.

          Most cited references34

          • Record: found
          • Abstract: found
          • Article: not found

          Leukocyte count and coronary heart disease: implications for risk assessment.

          Inflammation is a key feature of atherosclerosis and its clinical manifestations. The leukocyte count is a marker of inflammation that is widely available in clinical practice. This paper reviews the available epidemiologic evidence for a relationship between the leukocyte count and coronary heart disease (CHD). Numerous epidemiologic and clinical studies have shown leukocytosis to be an independent predictor of future cardiovascular events, both in healthy individuals free of CHD at baseline and in patients with stable angina, unstable angina, or a history of myocardial infarction. This relationship has been observed in prospective and retrospective cohort studies, as well as in case-control studies. It is strong, consistent, temporal, dose-dependent, and biologically plausible. The relationship persists after adjustment for multiple CHD risk factors, including smoking. Elevated differential cell counts, including eosinophil, neutrophil, and monocyte counts, also predict the future incidence of CHD. Leukocytosis affects CHD through multiple pathologic mechanisms that mediate inflammation, cause proteolytic and oxidative damage to the endothelial cells, plug the microvasculature, induce hypercoagulability, and promote infarct expansion. In summary, leukocytosis has been consistently shown to be an independent risk factor and prognostic indicator of future cardiovascular outcomes, regardless of disease status. The leukocyte count is inexpensive, reliable, easy to interpret, and ordered routinely in inpatient and outpatient settings. However, its diagnostic and prognostic utility in CHD is widely unappreciated. Further studies are needed to assess the true impact of leukocytosis on CHD, compare it with other inflammatory markers such as C-reactive protein and lipoprotein phospholipase A(2) levels, and promote its use in CHD prediction.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The neuroprogressive nature of major depressive disorder: pathways to disease evolution and resistance, and therapeutic implications.

            In some patients with major depressive disorder (MDD), individual illness characteristics appear consistent with those of a neuroprogressive illness. Features of neuroprogression include poorer symptomatic, treatment and functional outcomes in patients with earlier disease onset and increased number and length of depressive episodes. In such patients, longer and more frequent depressive episodes appear to increase vulnerability for further episodes, precipitating an accelerating and progressive illness course leading to functional decline. Evidence from clinical, biochemical and neuroimaging studies appear to support this model and are informing novel therapeutic approaches. This paper reviews current knowledge of the neuroprogressive processes that may occur in MDD, including structural brain consequences and potential molecular mechanisms including the role of neurotransmitter systems, inflammatory, oxidative and nitrosative stress pathways, neurotrophins and regulation of neurogenesis, cortisol and the hypothalamic-pituitary-adrenal axis modulation, mitochondrial dysfunction and epigenetic and dietary influences. Evidence-based novel treatments informed by this knowledge are discussed.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Modulation of inflammation in brain: a matter of fat.

              Neuroinflammation is a host defense mechanism associated with neutralization of an insult and restoration of normal structure and function of brain. Neuroinflammation is a hallmark of all major CNS diseases. The main mediators of neuroinflammation are microglial cells. These cells are activated during a CNS injury. Microglial cells initiate a rapid response that involves cell migration, proliferation, release of cytokines/chemokines and trophic and/or toxic effects. Cytokines/chemokines stimulate phospholipases A2 and cyclooxygenases. This results in breakdown of membrane glycerophospholipids with the release of arachidonic acid (AA) and docosahexaenoic acid (DHA). Oxidation of AA produces pro-inflammatory prostaglandins, leukotrienes, and thromboxanes. One of the lyso-glycerophospholipids, the other products of reactions catalyzed by phospholipase A2, is used for the synthesis of pro-inflammatory platelet-activating factor. These pro-inflammatory mediators intensify neuroinflammation. Lipoxin, an oxidized product of AA through 5-lipoxygenase, is involved in the resolution of inflammation and is anti-inflammatory. Docosahexaenoic acid is metabolized to resolvins and neuroprotectins. These lipid mediators inhibit the generation of prostaglandins, leukotrienes, and thromboxanes. Levels of prostaglandins, leukotrienes, and thromboxanes are markedly increased in acute neural trauma and neurodegenerative diseases. Docosahexaenoic acid and its lipid mediators prevent neuroinflammation by inhibiting transcription factor NFkappaB, preventing cytokine secretion, blocking the synthesis of prostaglandins, leukotrienes, and thromboxanes, and modulating leukocyte trafficking. Depending on its timing and magnitude in brain tissue, inflammation serves multiple purposes. It is involved in the protection of uninjured neurons and removal of degenerating neuronal debris and also in assisting repair and recovery processes. The dietary ratio of AA to DHA may affect neurodegeneration associated with acute neural trauma and neurodegenerative diseases. The dietary intake of docosahexaenoic acid offers the possibility of counter-balancing the harmful effects of high levels of AA-derived pro-inflammatory lipid mediators.
                Bookmark

                Author and article information

                Journal
                Neuropsychiatr Dis Treat
                Neuropsychiatr Dis Treat
                Neuropsychiatric Disease and Treatment
                Neuropsychiatric Disease and Treatment
                Dove Medical Press
                1176-6328
                1178-2021
                2015
                04 September 2015
                : 11
                : 2309-2314
                Affiliations
                [1 ]Hurvitz Brain Sciences Program, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Toronto, ON, Canada
                [2 ]Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada
                [3 ]Ottawa Institute of Systems Biology and Neural Regeneration Laboratory, Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada
                [4 ]CIHR Training Program in Neurodegenerative Lipidomics, Department of Biochemistry, Microbiology, and Immunology, University of Ottawa, Ottawa, ON, Canada
                [5 ]Department of Psychiatry, University of Toronto, Toronto, ON, Canada
                [6 ]UHN Toronto Rehabilitation Institute, Toronto, ON, Canada
                Author notes
                Correspondence: Krista L Lanctôt, Sunnybrook Research Institute, Sunnybrook Health Sciences Centre, Room FG08, 2075 Bayview Avenue, Toronto, ON M4N 3M5, Canada, Fax +1 416 480 6022, Email krista.lanctot@ 123456sunnybrook.ca
                Article
                ndt-11-2309
                10.2147/NDT.S87111
                4567245
                26379437
                f9faabf0-0fd2-4d35-87ae-56bee3feb069
                © 2015 Mazereeuw et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Neurology
                depression,lipidomics,cardiovascular,inflammation,oxidative stress,biomarker,vascular depression
                Neurology
                depression, lipidomics, cardiovascular, inflammation, oxidative stress, biomarker, vascular depression

                Comments

                Comment on this article