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Sökning: AMNE:(MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Neurologi) > Olsson T

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1.
  • Bahmanyar, S., et al. (författare)
  • Cancer risk among patients with multiple sclerosis and their parents
  • 2009
  • Ingår i: Neurology. - Minneapolis, Minn. : Lancet Publications Inc.. - 0028-3878 .- 1526-632X. ; 72:13, s. 1170-1177
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: We investigated cancer risk among patients with multiple sclerosis (MS) and whether variation by age at MS diagnosis helps to elucidate mechanisms underlying the previously reported reduced cancer risk. We also studied cancer risk among parents to ascertain if MS susceptibility genes may confer protection against cancer in relatives. METHODS: Cox proportional hazards regression, adjusted for age, sex, area, and socioeconomic index, estimated cancer risk among 20,276 patients with MS and 203,951 individuals without MS, using Swedish general population register data. Similar analyses were conducted among 11,284 fathers and 12,006 mothers of patients with MS, compared with 123,158 fathers and 129,409 mothers of controls. RESULTS: With an average of 35 years of follow-up, there was a decreased overall cancer risk among patients with MS (hazard ratio = 0.91, 0.87-0.95). Increased risks were observed for brain tumors (1.44, 1.21-1.72) and urinary organ cancer (1.27, 1.05-1.53). Parents of patients with MS did not have a notably increased or decreased overall cancer risk. CONCLUSIONS: The reduction in cancer risk in patients with multiple sclerosis (MS) may result from behavioral change, treatment, or we speculate that some immunologic characteristics of MS disease activity improve antitumor surveillance. The lack of association among parents indicates that a simple inherited characteristic is unlikely to explain the reduced cancer risk among patients with MS. MS is associated with increased risk for some cancers, such as of urinary organs and brain tumors (although surveillance bias may be responsible).
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2.
  • Montgomery, Scott M., et al. (författare)
  • Maternal smoking during pregnancy and multiple sclerosis amongst offspring
  • 2008
  • Ingår i: European Journal of Neurology. - Oxford : Blackwell. - 1351-5101 .- 1468-1331. ; 15:12, s. 1395-1399
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: An association between parental smoking and multiple sclerosis (MS) in offspring has been reported. This study examined whether maternal smoking during pregnancy is associated with MS in offspring.METHODS: Swedish general population registers provided prospectively recorded information on maternal smoking during pregnancy. The study identified 143 cases with MS diagnosed by 2006 and 1730 matched controls. Subjects were born since 1982 and individually matched by year of birth, age, sex and region of residence. Conditional logistic regression assessed the association of maternal smoking with MS in offspring with adjustment for socioeconomic index.RESULTS: Maternal smoking during pregnancy was not associated with MS in offspring, with an odds ratio (and 95% confidence interval) of 0.96 (0.65-1.44). When stratified by paediatric or later MS onset there was no association with maternal smoking in either stratum.CONCLUSION: It is unlikely that smoking during pregnancy represents a risk for early-onset MS amongst offspring.
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3.
  • Petit, Géraldine, et al. (författare)
  • Review: The future of cell therapies and brain repair: Parkinson's disease leads the way.
  • 2014
  • Ingår i: Neuropathology & Applied Neurobiology. - : Wiley. - 1365-2990 .- 0305-1846. ; 40:1, s. 60-70
  • Forskningsöversikt (refereegranskat)abstract
    • During the past 40 years brain tissue grafting techniques have been used both to study fundamental neurobiological questions and to treat neurological diseases. Motor symptoms of Parkinson's disease are largely due to degeneration of midbrain dopamine neurones. Because the nigrostriatal pathology is relatively focused anatomically, Parkinson's disease is considered the ideal candidate for brain repair by neural grafting and dopamine neurone transplantation for it has led the way in the neural transplantation research field. In this mini-review, we briefly highlight four important areas of development. First, we describe marked functional benefits up to 18 years after transplantation surgery in patients with Parkinson's disease. This is proof-of-principle that, using optimal techniques and patient selection, grafted dopamine neurones can work in humans and the duration of the benefit exceeds placebo effects associated with surgery. Second, we describe that eventually protein aggregates containing α-synuclein, identical to Lewy bodies, develop inside foetal dopamine neurones transplanted to patients with Parkinson's disease. This gives clues about pathogenetic mechanisms operating in Parkinson's disease, and also raises the question whether neural graft function will eventually decline as the result of the disease process. Third, we describe new emerging sources of transplantable dopamine neurones derived from pluripotent stem cells or reprogrammed adult somatic cells. Fourth, we highlight an important European Union-funded multicentre clinical trial involving transplantation of foetal dopamine neurones in Parkinson's disease. We describe the design of this ongoing trial and how it can impact on the overall future of cell therapy in Parkinson's disease.
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6.
  • Seoane, Fernando, 1976-, et al. (författare)
  • Brain electrical impedance at various frequencies : the effect of hypoxia
  • 2004
  • Ingår i: Proceedings of the 26th Annual International Conference of the IEEE EMBS, San Francisco, CA, USA • September 1-5, 2004. - : IEEE Engineering in Medicine and Biology Society. - 0780384393 ; 3, s. 2322-5
  • Konferensbidrag (refereegranskat)abstract
    • Non-invasive multi-frequency measurements of transcephalic impedance, both reactance and resistance, can efficiently detect cell swelling of brain tissue and can be used for early detection of threatening brain damage. We have performed experiments on piglets to monitor transcephalic impedance during hypoxia. The obtained results have confirmed the hypothesis that changes in the size of cells modify the tissue impedance. During tissue inflammation after induced hypoxia, cerebral tissue exhibits changes in both reactance and resistance. Those changes are remarkably high, up to 71% over the baseline, and easy to measure especially at certain frequencies. A better understanding of the electrical behaviour of cerebral tissue during cell swelling would lead us to develop effective non-invasive clinical tools and methods for early diagnosis of cerebral edema and brain damage prevention.
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7.
  • Olsson, Tomas T., et al. (författare)
  • Delayed Clinical Manifestation of Parkinson's Disease Among Physically Active : Do Participants in a Long-Distance Ski Race Have a Motor Reserve?
  • 2020
  • Ingår i: Journal of Parkinson's Disease. - : IOS Press. - 1877-7171 .- 1877-718X. ; 10:1, s. 267-274
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Physical activity is associated with reduced risk of Parkinson's disease (PD). The explanations for this association are not completely elucidated. We use long-term PD-incidence data from long-distance skiers to study the relationship between exercise and PD.OBJECTIVE: We aimed to investigate if physical activity is associated with long-term lower risk of PD and if this association could be explained by physically active people being able to sustain more PD neuropathology before clinical symptoms, a motor reserve.METHODS: Using a prospective observational design, we studied whether long-distance skiers of the Swedish Vasaloppet (n = 197,685), exhibited reduced incidence of PD compared to matched individuals from the general population (n = 197,684) during 21 years of follow-up (median 10, interquartile range (IQR) 5-15 years).RESULTS: Vasaloppet skiers (median age 36.0 years [IQR 29.0-46.0], 38% women) had lower incidence of PD (HR: 0.71; 95 % CI 0.56-0.90) compared to non-skiers. When reducing risk for reverse causation by excluding PD cases within the first five years from race participation, there was still a trend for lower risk of PD (HR: 0.80; 95 % CI 0.62-1.03). Further, the PD prevalence converged between skiers and non-skiers after 15 years of follow-up, which is more consistent with a motor reserve in the physically active rather than neuroprotection.CONCLUSIONS: A physical active lifestyle is associated with reduced risk for PD. This association weakens with time and might be explained by a motor reserve among the physically active.
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8.
  • Roshanisefat, H., et al. (författare)
  • All-cause mortality following a cancer diagnosis amongst multiple sclerosis patients : a Swedish population-based cohort study
  • 2015
  • Ingår i: European Journal of Neurology. - : Blackwell Publishing. - 1351-5101 .- 1468-1331. ; 22:7, s. 1074-1080
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and purpose: A reduced cancer risk amongst patients with multiple sclerosis (MS) has been reported. Theoretically, this could represent a genuine reduction in risk or, alternatively, diagnostic neglect', where cancer is undiagnosed when symptoms are misattributed to MS.Objective: Assess all-cause mortality risk following a cancer diagnosis in patients with MS compared with a cohort without MS.Patients: A cohort of MS patients (n=19364) and a cohort of the general population (n=192519) were extracted from national Swedish registers from 1969 to 2005. All-cause mortality after cancer in MS was compared with the general population. Poisson regression analysis was conducted in the MS and non-MS cohorts separately. The models were adjusted for follow-up duration, year at entry, sex, region and socioeconomic index. The two cohorts were combined and differences in mortality risk were assessed using interaction testing.Results: The adjusted relative risk (and 95% confidence interval) for all-cause mortality following a cancer diagnosis in MS patients (compared with MS patients without cancer) is 3.06 (2.86-3.27; n=1768) and amongst those without MS 5.73 (5.62-5.85; n=24965). This lower magnitude mortality risk in the MS patients was confirmed by multiplicative interaction testing (P<0.001).Conclusions: A consistent pattern of lower magnitude of all-cause mortality risk following cancer in MS patients for a range of organ-specific cancer types was found. It suggests that cancer diagnoses tend not to be delayed in MS and diagnostic neglect is unlikely to account for the reduced cancer risk associated with MS. The lower magnitude cancer risk in MS may be due to disease-associated characteristics or exposures.
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9.
  • Roshanisefat, H., et al. (författare)
  • Multiple sclerosis clinical course and cardiovascular disease risk : Swedish cohort study
  • 2014
  • Ingår i: European Journal of Neurology. - : Wiley-Blackwell. - 1351-5101 .- 1468-1331. ; 21:11, s. 1353-e88
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and purpose: Cardiovascular disease (CVD) risk amongst multiple sclerosis (MS) patients appears raised, but few studies have examined CVD risk amongst an unselected MS patient group. MS course may be relevant for CVD risk. Our aim was to assess CVD risk and variation by course in MS patients.Methods: The Multiple Sclerosis Register identified 7667 patients who received an MS diagnosis between 1964 and 2005. They were matched by age, period, region and sex with 76045 members of the general population without MS using Swedish registers. Poisson regression compared the two cohorts to estimate the relative risk for CVD, overall, as well as grouped and individual CVD diagnoses.Results: MS patients had an increased adjusted relative risk (with 95% confidence intervals; number of MS cohort events) for CVD of 1.31 (1.22-1.41; n=847), with some variation by course: relapsing-remitting 1.38 (1.17-1.62; n=168); secondary progressive 1.30 (1.18-1.53; n=405) and primary progressive 1.15 (0.93-1.41; n=108). The association for the relapsing-remitting course was not significant after excluding the first year of follow-up. Overall incidence rates per 1000 person-years for CVD are 11.8 (11.06-12.66) for the MS cohort and 8.8 (8.60-9.05) for the non-MS cohort. The most pronounced association was for deep vein thrombosis: relapsing-remitting 2.16 (1.21-3.87; n=14), secondary progressive 3.41 (2.45-4.75; n=52) and primary progressive 3.57 (1.95-6.56; n=15). MS was associated with ischaemic stroke but largely during the first year of follow-up. MS was associated with a decreased relative risk for angina pectoris and atrial fibrillation.Conclusions: There is a significantly increased relative risk for CVD in MS, particularly for venous thromboembolic disorders in progressive MS, suggesting immobility as a possible factor. An increased frequency of ischaemic stroke in MS is most probably due to surveillance bias resulting from diagnostic investigations for MS. There is no increased relative risk for ischaemic heart disease in MS and atrial fibrillation appears to be less common than amongst the general population. Click for the corresponding questions to this CME article.
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10.
  • Christensen, JR, et al. (författare)
  • CSF inflammation and axonal damage are increased and correlate in progressive multiple sclerosis
  • 2013
  • Ingår i: Multiple sclerosis (Houndmills, Basingstoke, England). - : SAGE Publications. - 1477-0970 .- 1352-4585. ; 19:7, s. 877-884
  • Tidskriftsartikel (refereegranskat)abstract
    • The mechanism underlying disease progression in progressive multiple sclerosis (MS) is uncertain. Pathological studies found widespread inflammation in progressive MS brains correlating with disease progression and axonal damage. Objectives: To study cerebrospinal fluid (CSF) biomarkers and clarify whether inflammation and axonal damage are associated in progressive MS. Methods: Using enzyme-linked immunosorbent assay (ELISA), we analysed CSF from 40 secondary progressive (SPMS), 21 primary progressive (PPMS), and 36 relapsing–remitting (RRMS) and 20 non-inflammatory neurological disease (NIND) patients. Twenty-two of the SPMS patients participated in an MBP8298 peptide clinical trial and had CSF follow-up after one year. Results: Compared to NIND patients, inflammatory biomarkers osteopontin and matrix metalloproteinase-9 (MMP9) were increased in all MS patients while CXCL13 was increased in RRMS and SPMS patients. Biomarkers of axonal damage (NFL) and demyelination (MBP) were increased in all MS patients. In progressive MS patients CSF levels of osteopontin and CXCL13 correlated with NFL while osteopontin and MMP9 correlated with MBP. MBP8298 treatment did not affect the levels of the biomarkers after one year of treatment. All biomarkers were continuously increased after one year of follow-up except MBP, which decreased. Conclusion: CSF biomarkers of inflammation, axonal damage and demyelination are continuously increased in progressive MS patients and correlate. These findings parallel pathology studies, emphasise a relationship between inflammation, axonal damage and demyelination and support the use of CSF biomarkers in progressive MS clinical trials.
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