| 101. |
- Janszky, Imre, et al.
(författare)
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Hospitalization for depression is associated with an increased risk for myocardial infarction not explained by lifestyle, lipids, coagulation, and inflammation : The SHEEP study
- 2007
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Ingår i: Biological Psychiatry. - : Elsevier BV. - 0006-3223 .- 1873-2402. ; 62:1, s. 25-32
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundDepression is considered a risk factor for coronary heart disease (CHD) in initially CHD-free populations. Subclinical CHD or other somatic causes of depressive symptoms might account for the association, however.MethodsIn this case–control study, patients had had their first acute myocardial infarction (AMI). The study included 1799 cases, aged 45–70 years, and 2339, age-, gender-, and hospital-catchment-area-matched control subjects. We calculated odds ratios (OR) with 95% confidence intervals (CI) by multivariate logistic regressions to assess the AMI risk associated with a hospitalization for depression.ResultsForty-seven cases and 22 control subjects had been hospitalized for depression. After adjustment for matching criteria and socioeconomic status, the OR for AMI was 2.9 (1.8–4.9) for ever hospitalized for depression. Patients hospitalized for depression before or after the median time, 15 years and 2 months, between the first hospitalization for depression and AMI, were at similar risk. Adjustment for lifestyle, lipid profile, coagulation, inflammation, prior cardiovascular events, and comorbidity only partly decreased the observed association.ConclusionsDepression was associated with increased risk for AMI. Subclinical CHD or other somatic causes are unlikely to account for our findings, which also appear not to be explained by established risk factors for AMI.
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| 102. |
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| 103. |
- Johansson, Carolina, et al.
(författare)
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Seasonal affective disorder and the G-protein beta-3-subunit C825T polymorphism
- 2004
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Ingår i: Biological Psychiatry. - New York : Elsevier. - 0006-3223 .- 1873-2402. ; 55:3, s. 317-319
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Tidskriftsartikel (refereegranskat)abstract
- Background: Guanine nucleotide-binding proteins (G-proteins) have been implicated in affective disorders, with reports of altered signal transduction and G-protein levels. Association with seasonal affective disorder (SAD) has been found for the higher activity T-allele of the G-protein beta-3-subunit C825T polymorphism.Methods. European SAD patients (n = 159) and matched controls (n = 159) were genotyped for the C825T. Seasonality and diurnal preference were investigated in subsets of the material (n = 177 and 92, respectively).Results. We found no association between C825T and SAD (chi(2) = .09, p = .96) or seasonality (F = 1.76, p = .18). There was some evidence for an effect on diurnal preference but only in the control group (n = 46, t = - 2.8, Bonferroni corrected p = .045).Conclusions: These results suggest that the G-protein beta-3-subunit 825 T-allele does not play a major role in susceptibility to seasonal affective disorder in the population studied.
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| 104. |
- Johansson, Maurits, et al.
(författare)
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Development of Apathy, Anxiety, and Depression in Cognitively Unimpaired Older Adults : Effects of Alzheimer's Disease Pathology and Cognitive Decline
- 2022
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Ingår i: Biological Psychiatry. - : Elsevier BV. - 0006-3223 .- 1873-2402. ; 92:1, s. 34-43
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Tidskriftsartikel (refereegranskat)abstract
- Background: The impact of Alzheimer's disease (AD) pathology and cognitive deficits on longitudinal neuropsychiatric symptoms is unclear, especially in early disease stages. Methods: Cognitively unimpaired older adults (N = 356) enrolled in the prospective Swedish BioFINDER study were examined. Neuropsychiatric assessments encompassed the Apathy Evaluation Scale and the Hospital Anxiety and Depression Scale, performed biennially (together with tests of global cognition) for up to 8 years. Biomarkers were measured in cerebrospinal fluid or plasma at baseline. Magnetic resonance imaging quantified white matter lesions. We used linear mixed-effect models to test associations between baseline AD biomarkers (for amyloid-β [Aβ], tau, and neurodegeneration) and white matter lesions with longitudinal neuropsychiatric symptoms (apathy, anxiety, and depressive symptoms). We also tested associations between changes in cognition and changes in neuropsychiatric symptoms. Finally, we tested if change in cognition mediated the effects of different brain pathologies on neuropsychiatric symptoms. Results: Aβ pathology at baseline was associated with increasing levels of apathy (β = −0.284, p =.005) and anxiety (β = −0.060, p =.011) longitudinally. More rapid decline of cognition over time was related to increasing levels of apathy. The effects of baseline Aβ pathology on longitudinal apathy were partly mediated by changes in cognitive performance (proportion mediated 23%). Conclusions: Aβ pathology may drive the development of both apathy and anxiety in very early stages of AD, largely independent of cognitive change. The effect of Aβ on apathy is only partially conveyed by worse cognition. Together, these findings highlight certain neuropsychiatric symptoms as early manifestations of AD.
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