18
views
0
recommends
+1 Recommend
1 collections
    0
    shares

      To submit to Bentham Journals, please click here

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

      Severe Psychiatric Disorders in Mid-Life and Risk of Dementia in Late-Life (Age 65-84 Years): A Population Based Case-Control Study

      research-article

      Read this article at

      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

          Objective:

          To examine the association of mid-life exposure to several psychiatric disorders with the development of late-life dementia. Methods: A matched case-control study using Western Australian state-wide hospital inpatient, outpatient mental health and emergency records linked to death records. Incident dementia cases (2000-2009) aged 65 to 84 years were sex- and age-matched to an electoral roll control. Records as far back as 1970 were used to assess exposure to medical risk factors before age 65 years. Candidate psychiatric risk factors were required to be present at least 10 years before dementia onset to ensure direction of potential causality. Odds ratios were estimated using conditional logistic regression. Results: 13, 568 dementia cases (median age 78.7 years, 43.4 % male) were matched to a control. Depression, bipolar disorder, schizophrenia, anxiety disorder and alcohol dependence were found to be significant and independent risk factors for late-life dementia after adjusting for diabetes, heart disease, cerebrovascular disease and smoking risk factors. The effect of a history of depression, schizophrenia and alcohol dependency on dementia risk varied with age, being strongest for earlier onset late-life dementia and waning at older ages. Conclusion: Severe depression, anxiety disorder, bipolar disorder, schizophrenia and alcoholic dependency disorder treated by specialists in psychiatric facilities in mid-life are important risk factors for late-life dementia. These psychiatric conditions need to be considered in future studies of the risk and prevention of late-life dementia.

          Related collections

          Most cited references50

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

          Depression as a predictor for coronary heart disease. a review and meta-analysis.

          To review and quantify the impact of depression on the development of coronary heart disease (CHD) in initially healthy subjects. Cohort studies on depression and CHD were searched in MEDLINE (1966-2000) and PSYCHINFO (1887-2000), bibliographies, expert consultation, and personal reference files. Cohort studies with clinical depression or depressive mood as the exposure, and myocardial infarction or coronary death as the outcome. Information on study design, sample size and characteristics, assessment of depression, outcome, number of cases, crude and most-adjusted relative risks, and variables used in multivariate adjustments were abstracted. Eleven studies met the inclusion criteria. The overall relative risk [RR] for the development of CHD in depressed subjects was 1.64 (95% confidence interval [CI]=1.29-2.08, p<0.001). A sensitivity analysis showed that clinical depression (RR=2.69, 95% CI=1.63-4.43, p<0.001) was a stronger predictor than depressive mood (RR=1.49, 95% CI=1.16-1.92, p=0.02). It is concluded that depression predicts the development of CHD in initially healthy people. The stronger effect size for clinical depression compared to depressive mood points out that there might be a dose-response relationship between depression and CHD. Implications of the findings for a broader bio-psycho-social framework are discussed.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Depression is an inflammatory disease, but cell-mediated immune activation is the key component of depression.

            The first findings that depression is characterized by cell-mediated immune activation and inflammation were published between 1990-1993 (Maes et al.). Recently, it was reported that--based on meta-analysis results--depression is an inflammatory disorder because the plasma levels of two cytokines are increased, i.e. interleukin-(IL)-6 and tumor necrosis factor-α (TNFα). The same meta-analysis found that plasma IL-2 and interferon-(IFN)γ levels are not altered in depression, suggesting that there is no T cell activation in that illness. The present paper reviews the body of evidence that depression is accompanied by cell-mediated immune activation. The findings include: increased serum levels of the soluble IL-2 receptor (sIL-2R) and the sCD8 molecule; increased numbers and percentages of T cells bearing T cell activation markers, such as CD2+CD25+, CD3+CD25+, and HLA-DR+; increased stimulated production of IFNγ; higher neopterin and sTNFR-1 or sTNFR-2 levels; induction of indoleamine 2,3-dioxygenase (IDO) with lowered levels of plasma tryptophan and increased levels of tryptophan catabolites along the IDO pathway (TRYCATs); and glucocorticoid resistance in immune cells. Interferon-α (IFNα)-based immunotherapy shows that baseline and IFNα-induced activation of T cells, IDO activity and TRYCAT formation are related to the development of IFNα-induced depressive symptoms. Animal models of depression show that a cell-mediated immune response is related to the development of depression-like behavior. Antidepressants and mood stabilizers suppress different aspects of cell-mediated immunity and rather specifically target IFNγ production. This review shows that inflammation and cell-mediated immune activation are key factors in depression. Copyright © 2010 Elsevier Inc. All rights reserved.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Head injury as a risk factor for Alzheimer's disease: the evidence 10 years on; a partial replication.

              To determine, using a systematic review of case-control studies, whether head injury is a significant risk factor for Alzheimer's disease. We sought to replicate the findings of the meta-analysis of Mortimer et al (1991). A predefined inclusion criterion specified case-control studies eligible for inclusion. A comprehensive and systematic search of various electronic databases, up to August 2001, was undertaken. Two independent reviewers screened studies for eligibility. Fifteen case-control studies were identified that met the inclusion criteria, of which seven postdated the study of Mortimer et al. We partially replicated the results of Mortimer et al. The meta-analysis of the seven studies conducted since 1991 did not reach significance. However, analysis of all 15 case-control studies was significant (OR 1.58, 95% CI 1.21 to 2.06), indicating an excess history of head injury in those with Alzheimer's disease. The finding of Mortimer et al that head injury is a risk factor for Alzheimer's disease only in males was replicated. The excess risk of head injury in those with Alzheimer's disease is only found in males (males: OR 2.29, 95% CI 1.47 to 2.06; females: OR 0.91, 95% CI 0.56 to 1.47). This study provides support for an association between a history of previous head injury and the risk of developing Alzheimer's disease.
                Bookmark

                Author and article information

                Journal
                Curr Alzheimer Res
                Curr Alzheimer Res
                CAR
                Current Alzheimer Research
                Bentham Science Publishers
                1567-2050
                1875-5828
                September 2014
                September 2014
                : 11
                : 7
                : 681-693
                Affiliations
                [1 ]Centre for Population Health Research, Curtin University, Perth, Western Australia, Australia
                [2 ]School of Medicine & Pharmacology, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia, Australia
                [3 ]School of Surgery, University of Western Australia, Perth, Western Australia, Australia
                Author notes
                [* ]Address correspondence to this author at the Curtin University, Room 238, Building 400, GPO Box U1987, Perth Western Australia 6845; Tel: +61 8 9266 1852; Fax: +61 8 9266 1866; E-mail: r.zilkens@ 123456curtin.edu.au
                Article
                CAR-11-681
                10.2174/1567205011666140812115004
                4153082
                25115541
                7dc4b556-deb7-4d42-b87a-7739171d2b6c
                © 2014 Bentham Science Publishers

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                : 13 August 2013
                : 19 June 2014
                : 3 July 2014
                Categories
                Article

                Neurology
                alzheimer’s disease,anxiety disorder,bipolar disorder,case-control studies,dementia,depression,risk factors,schizophrenia.

                Comments

                Comment on this article