| 1. |
- Andrews, Gavin, et al.
(författare)
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Lifetime risk of depression: restricted to a minority or waiting for most?
- 2005
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Ingår i: The British journal of psychiatry : the journal of mental science. - : Royal College of Psychiatrists. - 0007-1250. ; 187, s. 495-6
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Forskningsöversikt (refereegranskat)abstract
- Depression remits and recurs, but among what proportion of the population? Retrospective surveys report the lifetime risk to be around 10%. A modelling study and two prospective studies concur that close to half the population can expect one or more episodes of depression in their lifetime.
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| 2. |
- Aronsson, Gunnar, et al.
(författare)
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A systematic review including meta-analysis of work environment and burnout symptoms
- 2017
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Ingår i: Bmc Public Health. - : Springer Science and Business Media LLC. - 1471-2458. ; 17:264
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Forskningsöversikt (refereegranskat)abstract
- Background: Practitioners and decision makers in the medical and insurance systems need knowledge on the relationship between work exposures and burnout. Many burnout studies -original as well as reviews-restricted their analyses to emotional exhaustion or did not report results on cynicism, personal accomplishment or global burnout. To meet this need we carried out this review and meta-analyses with the aim to provide systematically graded evidence for associations between working conditions and near-future development of burnout symptoms. Methods: A wide range of work exposure factors was screened. Inclusion criteria were: 1) Study performed in Europe, North America, Australia and New Zealand 1990-2013. 2) Prospective or comparable case control design. 3) Assessments of exposure (work) and outcome at baseline and at least once again during follow up 1-5 years later. Twenty-five articles met the predefined relevance and quality criteria. The GRADE-system with its 4-grade evidence scale was used. Results: Most of the 25 studies focused emotional exhaustion, fewer cynicism and still fewer personal accomplishment. Moderately strong evidence (grade 3) was concluded for the association between job control and reduced emotional exhaustion and between low workplace support and increased emotional exhaustion. Limited evidence (grade 2) was found for the associations between workplace justice, demands, high work load, low reward, low supervisor support, low co-worker support, job insecurity and change in emotional exhaustion. Cynicism was associated with most of these work factors. Reduced personal accomplishment was only associated with low reward. There were few prospective studies with sufficient quality on adverse chemical, biological and physical factors and burnout. Conclusion: While high levels of job support and workplace justice were protective for emotional exhaustion, high demands, low job control, high work load, low reward and job insecurity increased the risk for developing exhaustion. Our approach with a wide range of work exposure factors analysed in relation to the separate dimensions of burnout expanded the knowledge of associations, evidence as well as research needs. The potential of organizational interventions is illustrated by the findings that burnout symptoms are strongly influenced by structural factors such as job demands, support and the possibility to exert control.
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| 3. |
- Bornstein, N. M., et al.
(författare)
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Diabetes and the brain: issues and unmet needs
- 2014
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Ingår i: Neurological Sciences. - : Springer Science and Business Media LLC. - 1590-1874 .- 1590-3478. ; 35:7, s. 995-1001
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Forskningsöversikt (refereegranskat)abstract
- Diabetes mellitus (DM) is associated with an increased risk of mild cognitive impairment, dementia and stroke. The association between DM and dementia appears to be stronger for vascular cognitive impairment than for Alzheimer's disease, suggesting cerebrovascular disease may be an important factor in cognitive impairment in DM. Although the exact mechanisms by which DM affects the brain remain unclear, changes to brain vasculature, disturbances of cerebral insulin signaling, insulin resistance, glucose toxicity, oxidative stress, accumulation of advanced glycation end products, hypoglycemic episodes, and alterations in amyloid metabolism may all be involved. Cognitive impairment and dementia associated with DM may also be mediated via vascular risk factors, in particular brain ischemia, the occurrence of which can have an additive or synergistic effect with concomitant neurodegenerative processes. To date, no drug has been approved for the treatment of vascular dementia and there are no specific pharmacological treatments for preventing or reducing cognitive decline in patients with DM. Most focus has been on tighter management of vascular risk factors, although evidence of reduced cognitive decline through reducing blood pressure, lipid-lowering or tighter glycemic control is inconclusive. Tailored, multimodal therapies may be required to reduce the risk of cognitive dysfunction and decline in patients with DM. The use of pleiotropic drugs with multimodal mechanisms of action (e.g., cerebrolysin, Actovegin) may have a role in the treatment of cognitive dysfunction and their use may warrant further investigation in diabetic populations.
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| 4. |
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| 5. |
- O'Brien, John T, et al.
(författare)
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Clinical practice with anti-dementia drugs: a revised (second) consensus statement from the British Association for Psychopharmacology.
- 2011
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Ingår i: Journal of psychopharmacology (Oxford, England). - : SAGE Publications. - 1461-7285 .- 0269-8811. ; 25:8, s. 997-1019
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Forskningsöversikt (refereegranskat)abstract
- The British Association for Psychopharmacology (BAP) coordinated a meeting of experts to review and revise its first (2006) Guidelines for clinical practice with anti-dementia drugs. As before, levels of evidence were rated using accepted standards which were then translated into grades of recommendation A to D, with A having the strongest evidence base (from randomized controlled trials) and D the weakest (case studies or expert opinion). Current clinical diagnostic criteria for dementia have sufficient accuracy to be applied in clinical practice (B) and brain imaging can improve diagnostic accuracy (B). Cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) are effective for mild to moderate Alzheimer's disease (A) and memantine for moderate to severe Alzheimer's disease (A). Until further evidence is available other drugs, including statins, anti-inflammatory drugs, vitamin E and Ginkgo biloba, cannot be recommended either for the treatment or prevention of Alzheimer's disease (A). Neither cholinesterase inhibitors nor memantine are effective in those with mild cognitive impairment (A). Cholinesterase inhibitors are not effective in frontotemporal dementia and may cause agitation (A), though selective serotonin reuptake inhibitors may help behavioural (but not cognitive) features (B). Cholinesterase inhibitors should be used for the treatment of people with Lewy body dementias (Parkinson's disease dementia and dementia with Lewy bodies (DLB)), especially for neuropsychiatric symptoms (A). Cholinesterase inhibitors and memantine can produce cognitive improvements in DLB (A). There is no clear evidence that any intervention can prevent or delay the onset of dementia. Although the consensus statement focuses on medication, psychological interventions can be effective in addition to pharmacotherapy, both for cognitive and non-cognitive symptoms. Many novel pharmacological approaches involving strategies to reduce amyloid and/or tau deposition are in progress. Although results of pivotal studies are awaited, results to date have been equivocal and no disease-modifying agents are either licensed or can be currently recommended for clinical use.
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| 6. |
- Ritchie, K., et al.
(författare)
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Is late-onset Alzheimer's disease really a disease of midlife?
- 2015
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Ingår i: Alzheimer's & Dementia. - : Wiley. - 1552-5260 .- 1552-5279. ; 1:2, s. 122-130
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Forskningsöversikt (refereegranskat)abstract
- Introduction Increasing evidence suggests that Alzheimer's disease (AD) may begin decades before evidence of dementia, indicating that it may be a disorder of midlife rather than old age. Methods In the absence of long-term prospective studies from early adulthood specifically designed to address this question, a group of international experts examined evidence presently available from previous clinical and population studies to provide an evidence-based opinion as to whether such a change in conceptualization may be justified. Results Although still lacking confirmation from dedicated prospective biomarker studies, there is already considerable evidence to suggest both risk factor exposure and brain changes may be already present in midlife. Discussion Current evidence suggests (1) that a change in clinical approach notably involving promotion of cardiovascular health in persons with a family history of AD may considerably reduce disease risk and (2) that the development of biomarkers at this early stage will lead to the possibility of clinical trials at a much earlier stage. © 2015 The Authors. Published by Elsevier Inc.
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| 7. |
- Rockwood, Kenneth, et al.
(författare)
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The inclusion of cognition in vascular risk factor clinical practice guidelines.
- 2009
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Ingår i: Clinical interventions in aging. - 1176-9092. ; 4, s. 425-33
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Forskningsöversikt (refereegranskat)abstract
- BACKGROUND: People with vascular risk factors are at increased risk for cognitive impairment as well as vascular disease. The objective of this study was to evaluate whether vascular risk factor clinical practice guidelines consider cognition as an outcome or in connection with treatment compliance. METHODS: ARTICLES FROM PUBMED, EMBASE, AND THE COCHRANE LIBRARY WERE ASSESSED BY AT LEAST TWO REVIEWERS AND WERE INCLUDED IF: (1) Either hypertension, high cholesterol, diabetes, or atrial fibrillation was targeted; (2) The guideline was directed at physicians; (3) Adult patients (aged 19 years or older) were targeted; and (4) The guideline was published in English. Of 91 guidelines, most were excluded because they were duplicates, older versions, or focused on single outcomes. RESULTS: Of the 20 clinical practice guidelines that met inclusion criteria, five mentioned cognition. Of these five, four described potential treatment benefits but only two mentioned that cognition may affect compliance. No guidelines adequately described how to screen for cognitive impairment. CONCLUSION: Despite evidence that links cognitive impairment to vascular risk factors, only a minority of clinical practice guidelines for the treatment of vascular risk factors consider cognition as either an adverse outcome or as a factor to consider in treatment.
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| 8. |
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| 9. |
- Sjögren, Magnus, et al.
(författare)
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Cholesterol and Alzheimer's disease--is there a relation?
- 2006
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Ingår i: Mechanisms of ageing and development. - : Elsevier BV. - 0047-6374. ; 127:2, s. 138-47
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Forskningsöversikt (refereegranskat)abstract
- The predominating theory on the pathophysiology of Alzheimer's disease (AD) concerns the mis-metabolism of amyloid precursor protein (APP). As a result of this mis-metabolism, there is an increased production of the 42 amino acid form of beta-amyloid (Abeta42) that rapidly will form oligomers that initiates a cascade of events leading to the accumulation of amyloid plaques. Commonly recognised as vascular factors, hypertension, hypercholesterolemia and diabetes and the inheritance of the epsilon4 allele of the APOE gene, are also risk factors for AD. These risks have been found to promote the production of Abeta42. An association between cholesterol and the development of AD was suggested in the early 1990s and ever since, an increasing amount of research has confirmed that there is a link between cholesterol and the development of AD. A high cholesterol levels in mid-life is a risk for AD and statins, i.e., cholesterol-lowering drugs, reduce this risk. Statins may not only inhibit enzymes involved in the endogenous synthesis of cholesterol but also affect enzymes involved in Abeta metabolism, i.e., alpha-secretase and beta-secretase. This normalises the breakdown of APP thereby promoting the non-amyloidogenic pathway. In this review, investigations focusing on cholesterol and Alzheimer's disease are presented.
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