| 1. |
- Bauer, I. E., et al.
(author)
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Inflammatory mediators of cognitive impairment in bipolar disorder
- 2014
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In: Journal of Psychiatric Research. - : Elsevier BV. - 0022-3956. ; 56, s. 18-27
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Journal article (peer-reviewed)abstract
- Objectives: Recent studies have pointed to neuroinflammation, oxidative stress and neurotrophic factors as key mediators in the pathophysiology of mood disorders. Little is however known about the cascade of biological episodes underlying the cognitive deficits observed during the acute and euthymic phases of bipolar disorder (BD). The aim of this review is to assess the potential association between cognitive impairment and biomarkers of inflammation, oxidative stress and neurotrophic activity in BD. Methods: Scopus (all databases), Pubmed and Ovid Medline were systematically searched with no language or year restrictions, up to November 2013, for human studies that collected both inflammatory markers and cognitive data in BD. Selected search terms were bipolar disorder, depression, mania, psychosis, inflammatory, cognitive and neurotrophic. Results: Ten human studies satisfied the criteria for consideration. The findings showed that high levels of peripheral inflammatory-cytokine, oxidative stress and reduced brain derived neurotrophic factor (BDNF) levels were associated with poor cognitive performance. The BDNF val66met polymorphism is a potential vulnerability factor for cognitive impairment in BD. Conclusions: Current data provide preliminary evidence of a link between the cognitive decline observed in BD and mechanisms of neuroinflammation and neuroprotection. The identification of BD specific inflammatory markers and polymorphisms in inflammatory response genes may be of assistance for therapeutic intervention. (C) 2014 Elsevier Ltd. All rights reserved.
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| 2. |
- Pascoe, Michaela C., et al.
(author)
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A systematic review of randomised control trials on the effects of yoga on stress measures and mood
- 2015
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In: Journal of Psychiatric Research. - : Elsevier BV. - 0022-3956. ; 68, s. 270-282
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Journal article (peer-reviewed)abstract
- Stress related disorders such as depression and anxiety are leading sources of disability worldwide, and current treatment methods such as conventional antidepressant medications are not beneficial for all individuals. There is evidence that yoga has mood-enhancing properties possibly related to its inhibitory effects on physiological stress and inflammation, which are frequently associated with affective disorders. However the biological mechanisms via which yoga exerts its therapeutic mood-modulating effects are largely unknown. This systematic review investigates the effects of yoga on sympathetic nervous system and hypothalamic pituitary adrenal axis regulation measures. It focuses on studies collecting physiological parameters such as blood pressure, heart rate, cortisol, peripheral cytokine expression and/or structural and functional brain measures in regions involved in stress and mood regulation. Overall the 25 randomised control studies discussed provide preliminary evidence to suggest that yoga practice leads to better regulation of the sympathetic nervous system and hypothalamic-pituitary-adrenal system, as well as a decrease in depressive and anxious symptoms in a range of populations. Further research is warranted to confirm these preliminary findings and facilitate implementation in clinical settings. (C) 2015 Elsevier Ltd. All rights reserved.
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| 3. |
- Pascoe, Michaela C., et al.
(author)
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Albumin and depression in elderly stroke survivors: An observational cohort study
- 2015
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In: Psychiatry Research. - : Elsevier BV. - 0165-1781 .- 1872-7123. ; 230:2, s. 658-63
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Journal article (peer-reviewed)abstract
- Abstract BACKGROUND/OBJECTIVES: Post-stroke depression affects approximately one third of stroke survivors. In non-stroke affected populations, depressive symptomatology is associated with hypoalbuminemia. This is also common among stroke survivors and associated with poor outcome and increased mortality. The role of stroke-associated hypoalbuminemia in post-stroke depression is not clear. We aimed to explore the relationship between serum albumin and post-stroke depression, as measured 20 months post-stroke. SUBJECTS/METHODS: Observational cohort study of elderly Swedish patients drawn from the 'Gothenburg 70+ Stroke Study' (n=149) and assessed at 20 months after stroke onset. Serum albumin was drawn from venous blood and analysed with gas chromatography/mass spectrometry. Depressive symptomatology was assessed using the Montgomery-Åsberg Depression Rating Scale (MADRS) and functional impairment was assessed using the Barthel Index. RESULTS: Analysis of covariance analysis showed that serum albumin levels were associated with depressive symptoms at 20 months after stroke. Multivariate analysis of covariance showed that disability scores at 3 days were associated with depressive symptoms at 20 months after stroke and after accounting for the age covariate. Stroke survivors were not clinically deficient in serum albumin. CONCLUSIONS: Low serum albumin appears to be associated with depressive symptoms in elderly individuals long term post-stroke
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| 4. |
- Pascoe, Michaela C., et al.
(author)
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Folate and MMA predict cognitive impairment in elderly stroke survivors: A cross sectional study
- 2016
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In: Psychiatry Research. - : Elsevier BV. - 0165-1781. ; 243, s. 49-52
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Journal article (peer-reviewed)abstract
- Elderly stroke survivors are at risk of malnutrition and long-term cognitive impairment. Vitamin B-related metabolites, folate and methylmalonic acid, have been implicated in cognitive function. We conducted a study exploring the relationship between blood folate, methylmalonic acid and post-stroke cognitive impairment. This is a cross sectional study of elderly Swedish patients (n=149) 20 months post-stroke, assessed using the Mini Mental State Examination, serum blood levels of methylmalonic acid and red blood cell levels of folate. Linear modeling indicated that low levels of blood folate and elevated methylmalonic acid significantly contributed to cognitive impairment in stroke survivors. Half of the stroke survivors were shown to have folate deficiency at 20 months after stroke. Folate deficiency is common long term after stroke and both low folate and elevated methylmalonic acid appear to be associated with long term cognitive impairment, in elderly Swedish stroke survivors. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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| 5. |
- Stokowska, Anna, et al.
(author)
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Complement peptide C3a stimulates neural plasticity after experimental brain ischaemia.
- 2017
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In: Brain. - : Oxford University Press. - 0006-8950 .- 1460-2156. ; 140:2
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Journal article (peer-reviewed)abstract
- Ischaemic stroke induces endogenous repair processes that include proliferation and differentiation of neural stem cells and extensive rewiring of the remaining neural connections, yet about 50% of stroke survivors live with severe long-term disability. There is an unmet need for drug therapies to improve recovery by promoting brain plasticity in the subacute to chronic phase after ischaemic stroke. We previously showed that complement-derived peptide C3a regulates neural progenitor cell migration and differentiation in vitro and that C3a receptor signalling stimulates neurogenesis in unchallenged adult mice. To determine the role of C3a-C3a receptor signalling in ischaemia-induced neural plasticity, we subjected C3a receptor-deficient mice, GFAP-C3a transgenic mice expressing biologically active C3a in the central nervous system, and their respective wild-type controls to photothrombotic stroke. We found that C3a overexpression increased, whereas C3a receptor deficiency decreased post-stroke expression of GAP43 (P < 0.01), a marker of axonal sprouting and plasticity, in the peri-infarct cortex. To verify the translational potential of these findings, we used a pharmacological approach. Daily intranasal treatment of wild-type mice with C3a beginning 7 days after stroke induction robustly increased synaptic density (P < 0.01) and expression of GAP43 in peri-infarct cortex (P < 0.05). Importantly, the C3a treatment led to faster and more complete recovery of forepaw motor function (P < 0.05). We conclude that C3a-C3a receptor signalling stimulates post-ischaemic neural plasticity and intranasal treatment with C3a receptor agonists is an attractive approach to improve functional recovery after ischaemic brain injury.media-1vid110.1093/brain/aww314_video_abstractaww314_video_abstract.
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