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Sökning: WFRF:(Freund Levi Yvonne)

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21.
  • Freund-Levi, Yvonne, 1956-, et al. (författare)
  • Galantamine versus risperidone treatment of neuropsychiatric symptoms in patients with probable dementia : an open randomized trial
  • 2014
  • Ingår i: The American journal of geriatric psychiatry. - : Elsevier. - 1064-7481 .- 1545-7214. ; 22:4, s. 341-248
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To examine the effects of galantamine and risperidone on neuropsychiatric symptoms in dementia (NPSD) and global function.METHODS: Using a randomized, controlled and open-blind, one-center trial at an in- and outpatient clinic at a university hospital, we studied 100 adults with probable dementia and NPSD. Participants received galantamine (N = 50, target dose 24 mg) or risperidone (N = 50, target dose 1.5 mg) for 12 weeks. The primary outcome was effects on NPSD assessed by the Neuropsychiatric Inventory (NPI). Secondary measures included the Mini-Mental State Examination (MMSE), Clinical Dementia Rating, Clinical Global Impression, and Simpson Angus scales. All tests were performed before and after treatment.RESULTS: Outcome measures were analyzed using analysis of covariance. Ninety-one patients (67% women, mean age 79 ± 7.5 years) with initial NPI score of 51.0 (± 25.8) and MMSE of 20.1 (± 4.6) completed the trial. Both galantamine and risperidone treatments resulted in improved NPSD symptoms and were equally effective in treating several NPI domains. However, risperidone showed a significant treatment advantage in the NPI domains irritation and agitation, F(1, 97) = 5.2, p = 0.02. Galantamine treatment also ameliorated cognitive functions where MMSE scores increased 2.8 points compared with baseline (95% confidence interval: 1.96-3.52). No treatment-related severe side effects occurred.CONCLUSIONS: These results support that galantamine, with its benign safety profile, can be used as first-line treatment of NPSD symptoms, unless symptoms of irritation and agitation are prominent, where risperidone is more efficient.
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22.
  • Freund-Levi, Yvonne, 1956-, et al. (författare)
  • Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease : OmegAD study - A randomized double-blind trial
  • 2006
  • Ingår i: Archives of Neurology. - : American Medical Association (AMA). - 0003-9942 .- 1538-3687. ; 63:10, s. 1402-1408
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Epidemiologic and animal studies have suggested that dietary fish or fish oil rich in omega-3 fatty acids, for example, docosahexaenoic acid and eicosapentaenoic acid, may prevent Alzheimer disease (AD). Objective: To determine effects of dietary omega-3 fatty acid supplementation on cognitive functions in patients with mild to moderate AD. Design: Randomized, double-blind, placebo-controlled clinical trial. Participants: Two hundred four patients with AD (age range [mean +/- SD], 74 +/- 9 years) whose conditions were stable while receiving acetylcholine esterase inhibitor treatment and who had a Mini-Mental State Examination (MMSE) score of 15 points or more were randomized to daily intake of 1.7 g of docosahexaenoic acid and 0.6 g of eicosapentaenoic acid (omega-3 fatty acid-treated group) or placebo for 6 months, after which all received omega-3 fatty acid supplementation for 6 months more. Main Outcome Measures: The primary outcome was cognition measured with the MMSE and the cognitive portion of the Alzheimer Disease Assessment Scale. The secondary outcome was global function as assessed with the Clinical Dementia Rating Scale; safety and tolerability of omega-3 fatty acid supplementation; and blood pressure determinations. Results: One hundred seventy-four patients fulfilled the trial. At baseline, mean values for the Clinical Dementia Rating Scale, MMSE, and cognitive portion of the Alzheimer Disease Assessment Scale in the 2 randomized groups were similar. At 6 months, the decline in cognitive functions as assessed by the latter 2 scales did not differ between the groups. However, in a subgroup (n=32) with very mild cognitive dysfunction (MMSE > 27 points), a significant (P <.05) reduction in MMSE decline rate was observed in the omega-3 fatty acid-treated group compared with the placebo group. A similar arrest in decline rate was observed between 6 and 12 months in this placebo subgroup when receiving omega-3 fatty acid supplementation. The omega-3 fatty acid treatment was safe and well tolerated. Conclusions: Administration of omega-3 fatty acid in patients with mild to moderate AD did not delay the rate of cognitive decline according to the MMSE or the cognitive portion of the Alzheimer Disease Assessment Scale. However, positive effects were observed in a small group of patients with very mild AD (MMSE > 27 points).
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23.
  • Freund-Levi, Yvonne (författare)
  • Omega-3 fatty acid treatment in mild to moderate Alzheimer's disease : results from the OmegAD study
  • 2008
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Alzheimer's disease (AD) is a major public health concern in all countries with an increasing prevalence. It is expected to quadruple by the year 2047. AD is a progressive neurodegenerative disease with a multifactorial origin, where a body of genetic and biochemical evidence, inflammatory aspects as well as the pivotal role of soluble amyloid β peptide (Aβ) may be the proximate cause of synaptic injuries and neuronal death leading to cognitive and neuropsychiatric decline leading to suffering in both the patient and the caregiver. Today there is no cure for AD, albeit we have access to pharmacotherapy that might improve cognitive and neuropsychiatric symptoms initially in the course of the disease. However, AD continues to progress despite treatment. It is therefore of utter importance to find other pharmacological strategies that might postpone the development of AD and also slow down the cognitive and neuropsychiatric decline in manifest AD. AD patients display lower levels of the omega-3 fatty acid (n-3 FA) docosahexaenoic acid (DHA) in both plasma and brain tissues as compared to age matched controls. Furthermore, epidemiological and animal studies suggest that high intake of DHA might have preventive properties against AD. Little is known, however, of the effects of n-3 FA on AD. Therefore we have conducted the first one year long randomised placebo controlled double-blind trial with six months administration of 2.3 g/day n-3 FA (1.7 g DHA + 0.6 g EPA) or placebo (linoleic acid, LA) followed by six months administration of n-3 FA to patients with mild to moderate AD. In total 204 patients with mild to moderate AD already on stable medication with acetylcholinesterase inhibitors (AChEI) were included. One hundred and seventy four patients fulfilled the trial and the Papers I, II and IV are based on these patients. In a subgroup of these patients lumbar puncture was performed (Paper III). All patients were followed for one year with cognitive, neuropsychiatric and functional evaluations as well as blood tests. In Paper I we conclude that n-3 FA treatment did not delay the rate of cognition as measured with the Mini Mental State Examination (MMSE) and the cognitive subscale of the Alzheimer's disease Assessment Scale (ADAS-cog) nor global status measured with the Clinical Dementia Rating scale (CDR). However, positive effects on cognition were observed in a small group of patients with very mild AD (MMSE >27). Safety and tolerability was good as was compliance measured with plasma levels of DHA, EPA and LA. In Paper II we addressed the effects of supplementation of n-3 FA on the neuropsychiatric, behavioural and functional symptoms using the Neuropsychiatric Inventory (NPI) and the Montgomery Åsberg Depression Rating scale (MADRS). Disability Assessment for Dementia (DAD) and Care givers burden (CGB). The relationship with APOE genotype was assessed. There was no overall treatment effect on neuropsychiatric, behavioural and functional symptoms, but n-3 FA appeared to have positive treatment effects on depression in non-APOEε4 carriers and in agitation in APOE ε4 carriers. In Paper III inflammatory markers in plasma (hs-CRP, IL-6, TNF-α and sIL-RII) and cerebrospinal fluid (CSF, IL-6, TNF-α and sIL-RII) and biological AD markers in CSF (Aβ42, T-tau and P-tau) were analyzed in a subgroup of 35 patients. A correlation at baseline between Aβ42 and sIL-RII was detected albeit no n-3 FA treatment effects were found in neither inflammatory nor biological AD markers. In Paper IV we investigated the hypothesis that supplementation with n-3 FA would affect appetite and weight in relation to inflammatory biomarkers and to APOE ε4 carrier ship. Mean weight and Body Mass Index (BMI) increased at 6 and 12 months in the n-3 FA group. When the placebo group was administered n-3 FA for six months, the weight and BMI also increased significantly within the group. However, there was no significant treatment effect on weight and BMI between the groups. Not carrying the APOEε4 allele and increased DHA were independently associated with weight gain. Caregiver s assessed appetite improved in the n-3 FA treatment group over the treatment period. In conclusion, our study gives some evidence that supplementation with 2.3 g/day n-3 FA to patients with mild to moderate AD may have effects on cognition in the early phases of AD, may reduce depression and agitation depending on APOE ε4 status and increase body weight loss in patients with mild to moderate AD. No effect on possible neuroinflammation in subjects with AD was observed. Supplementation with n-3 FA may be a strategy to add to lifestyle prevention for postponing early cognitive symptoms in AD but more research is needed.
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24.
  • Freund-Levi, Yvonne, 1956-, et al. (författare)
  • Omega-3 supplementation in mild to moderate Alzheimer's disease : effects on neuropsychiatric symptoms
  • 2008
  • Ingår i: International Journal of Geriatric Psychiatry. - : Wiley. - 0885-6230 .- 1099-1166. ; 23:2, s. 161-169
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Epidemiological and animal studies have suggested that dietary fish or fish oil rich in omega-3 fatty acids (ω3), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), may have effects in psychiatric and behavioral symptoms in Alzheimer's disease (AD). An association with APOEω4 carriers and neuropsychiatric symptoms in AD has also been suggested. Objective: To determine effects of dietary ω3 supplementation to AD patients with mild to moderate disease on psychiatric and behavioral symptoms, daily functions and a possible relation to APOEgenotype. Methods: Randomized, double-blind, placebo-controlled clinical trial where 204 AD patients (74 ± 9 years) with acetylcholine esterase inhibitor treatment and a MMSE >15 points were randomized to daily intake of 1.7 g DHA and 0.6 g EPA (ω3 group) or placebo for 6 months. Then, all received the ω3 supplementation for 6 more months. Neuropsychiatric symptoms were measured with Neuropsychiatric Inventory (NPI) and Montgomery Åsberg Depression Scale (MADRS). Caregivers burden and activities of daily living (Disability Assessment for Dementia, DAD) were also assessed. Results: One hundred and seventy-four patients fulfilled the trial. 72% were APOEω4 carriers. No significant overall treatment effects on neuropsychiatric symptoms, on activities of daily living or on caregiver's burden were found. However, significant positive treatment effects on the scores in the NPI agitation domain in APOEω4 carriers (p = 0.006) and in MADRS scores in non-APOEω4 carriers (p = 0.005) were found. Conclusions: Supplementation with ω3 in patients with mild to moderate AD did not result in marked effects on neuropsychiatric symptoms except for possible positive effects on depressive symptoms (assessed by MADRS) in non-APOEω4 carriers and agitation symptoms (assessed by NPI) in APOEω4 carriers. ClinicalTrials.gov identifier: NCT00211159.
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25.
  • Freund-Levi, Yvonne, 1956-, et al. (författare)
  • Response to Bogaiksy's Letter to the Editor
  • 2014
  • Ingår i: The American journal of geriatric psychiatry. - : Elsevier. - 1064-7481 .- 1545-7214. ; 22:9, s. 951-951
  • Tidskriftsartikel (refereegranskat)abstract
    • Refers to Michael Bogaisky, Galantamine Versus Risperidone Treatment of Neuropsychiatric Symptoms in Patients with Probable Dementia: An Open Randomized Trial, The American Journal of Geriatric Psychiatry, Volume 22, Issue 9, September 2014, Pages 951.
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26.
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27.
  • Freund-Levi, Yvonne, 1956-, et al. (författare)
  • Transfer of omega-3 fatty acids across the blood-brain barrier after dietary supplementation with a docosahexaenoic acid-rich omega-3 fatty acid preparation in patients with Alzheimer's disease : the OmegAD study
  • 2014
  • Ingår i: Journal of Internal Medicine. - : Blackwell Publishing. - 0954-6820 .- 1365-2796. ; 275:4, s. 428-436
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Little is known about the transfer of essential fatty acids (FAs) across the human blood-brain barrier (BBB) in adulthood. In this study, we investigated whether oral supplementation with omega-3 (n-3) FAs would change the FA profile of the cerebrospinal fluid (CSF).METHODS: A total of 33 patients (18 receiving the n-3 FA supplement and 15 receiving placebo) were included in the study. These patients were participants in the double-blind, placebo-controlled randomized OmegAD study in which 204 patients with mild Alzheimer's disease (AD) received 2.3 g n-3 FA [high in docosahexaenoic acid (DHA)] or placebo daily for 6 months. CSF FA levels were related to changes in plasma FA and to CSF biomarkers of AD and inflammation.RESULTS: At 6 months, the n-3 FA supplement group displayed significant increases in CSF (and plasma) eicosapentaenoic acid (EPA), DHA and total n-3 FA levels (P < 0.01), whereas no changes were observed in the placebo group. Changes in CSF and plasma levels of EPA and n-3 docosapentaenoic acid were strongly correlated, in contrast to those of DHA. Changes in DHA levels in CSF were inversely correlated with CSF levels of total and phosphorylated tau, and directly correlated with soluble interleukin-1 receptor type II. Thus, the more DHA increased in CSF, the greater the change in CSF AD/inflammatory biomarkers.CONCLUSIONS: Oral supplementation with n-3 FAs conferred changes in the n-3 FA profile in CSF, suggesting transfer of these FAs across the BBB in adults.
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28.
  • Funkquist, Anders, 1977-, et al. (författare)
  • Higher CSF/serum free-T4 ratio is associated with improvement of quality of life during treatment with L-thyroxine
  • 2023
  • Ingår i: Journal of Neuroendocrinology. - : Wiley-Blackwell Publishing Inc.. - 0953-8194 .- 1365-2826. ; 35:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Up to 20% of individuals with primary hypothyroidism treated with L-thyroxine still suffer from severe symptoms. These are supposedly brain derived and involve both cognitive and emotional domains. Previously, no consistent relationship has been found between thyroid hormones (TH) or TSH levels in blood and quality of life (QoL). Recently, we reported an association between cerebrospinal fluid (CSF)/serum free-thyroxine (f-T4) ratio and QoL, in juvenile hypothyroid patients. Here, we investigated if CSF/serum f-T4 ratio and QoL estimates correlate also during L-thyroxine treatment. Moreover, the CSF biomarker neurogranin (Ng) was used as a biomarker for synaptic function and integrity in clinical research. Ng is partially controlled by TH and therefore we investigated the relationship between QoL parameters and Ng levels. Patients diagnosed with primary hypothyroidism were investigated using vital parameters, serum and CSF analyses of TH, TSH, Ng and QoL questionnaires. Similar procedures were performed after 6 months of treatment. The most marked associations with QoL were found for CSF/serum f-T4 ratio, which was strongly related to several QoL parameters such as the mental subscore of SF-36 (r = 0.83, p < .0005). Ng, which did not differ from that in our healthy controls, was lower in some patients during treatment and higher in others. However, the change in Ng during treatment was significantly correlated with QoL parameters including the mental subscore of SF-36 (r = -0.86, p < .0001). In addition, the CSF/serum f-T4 ratio correlated with the change in Ng (r = -0.75, p = .001). Our results suggest that the ratio between CSF and serum f-T4 is an important biomarker for QoL during treatment of patients with primary hypothyroidism, so far in research, but in the future maybe also in clinical settings. Moreover, this ratio also correlates with the changes in Ng levels during L-thyroxine treatment, further supporting the impact of the TH balance between serum and CSF on QoL.
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29.
  • Ghafouri, Bijar, et al. (författare)
  • Swedish Chronic Pain Biobank : protocol for a multicentre registry and biomarker project
  • 2022
  • Ingår i: BMJ Open. - : BMJ Publishing Group Ltd. - 2044-6055. ; 12:11
  • Tidskriftsartikel (refereegranskat)abstract
    • INTRODUCTION: About 20% of the adult population have chronic pain, often associated with psychological distress, sick leave and poor health. There are large variations in the clinical picture. A biopsychosocial approach is used in investigation and treatment. The concept of personalised medicine, that is, optimising medication types and dosages for individual patients based on biomarkers and other patient-related factors, has received increasing attention in different diseases but used less in chronic pain. This cooperative project from all Swedish University Hospitals will investigate whether there are changes in inflammation and metabolism patterns in saliva and blood in chronic pain patients and whether the changes correlate with clinical characteristics and rehabilitation outcomes.METHODS AND ANALYSIS: Patients at multidisciplinary pain centres at University Hospitals in Sweden who have chosen to participate in the Swedish Quality Registry for Pain Rehabilitation and healthy sex-matched and age-matched individuals will be included in the study. Saliva and blood samples will be collected in addition to questionnaire data obtained from the register. From the samples, proteins, lipids, metabolites and micro-RNA will be analysed in relation to, for example, diagnosis, pain characteristics, psychological distress, body weight, pharmacological treatment and clinical rehabilitation results using advanced multivariate data analysis and bioinformatics.ETHICS AND DISSEMINATION: The study is approved by the Swedish Ethical Review Authority (Dnr 2021-04929) and will be conducted in accordance with the declaration of Helsinki.The results will be published in open access scientific journals and in popular scientific relevant journals such as those from patient organisations. Data will be also presented in scientific meetings, meeting with healthcare organisations and disseminated in different lecturers at the clinics and universities.
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30.
  • Hall, Anette, et al. (författare)
  • Predicting Progression from Cognitive Impairment to Alzheimer's Disease with the Disease State Index
  • 2015
  • Ingår i: Current Alzheimer Research. - : Bentham Science Publishers Ltd.. - 1875-5828 .- 1567-2050. ; 12:1, s. 69-79
  • Tidskriftsartikel (refereegranskat)abstract
    • We evaluated the performance of the Disease State Index (DSI) method when predicting progression to Alzheimer's disease (AD) in patients with subjective cognitive impairment (SCI), amnestic or non-amnestic mild cognitive impairment (aMCI, naMCI). The DSI model measures patients' similarity to diagnosed cases based on available data, such as cognitive tests, the APOE genotype, CSF biomarkers and MRI. We applied the DSI model to data from the DE-SCRIPA cohort, where non-demented patients (N=775) with different subtypes of cognitive impairment were followed for 1 to 5 years. Classification accuracies for the subgroups were calculated with the DSI using leave-one-out cross-validation. The DSI's classification accuracy in predicting progression to AD was 0.75 (AUC=0.83) in the total population, 0.70 (AUC=0.77) for aMCI and 0.71 (AUC=0.76) for naMCI. For a subset of approximately half of the patients with high or low DSI values, accuracy reached 0.86 (all), 0.78 (aMCI), and 0.85 (naMCI). For patients with MRI or CSF biomarker data available, they were 0.78 (all), 0.76 (aMCI) and 0.76 (naMCI), while for clear cases the accuracies rose to 0.90 (all), 0.83 (aMCI) and 0.91 (naMCI). The results show that the DSI model can distinguish between clear and ambiguous cases, assess the severity of the disease and also provide information on the effectiveness of different biomarkers. While a specific test or biomarker may confound analysis for an individual patient, combining several different types of tests and biomarkers could be able to reveal the trajectory of the disease and improve the prediction of AD progression.
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