uu.seUppsala universitets publikasjoner
Endre søk
Link to record
Permanent link

Direct link
BETA
Basun, H
Alternativa namn
Publikasjoner (10 av 36) Visa alla publikasjoner
Jernerén, F., Cederholm, T., Refsum, H., Smith, A. D., Turner, C., Palmblad, J., . . . Freund-Levi, Y. (2019). Homocysteine Status Modifies the Treatment Effect of Omega-3 Fatty Acids on Cognition in a Randomized Clinical Trial in Mild to Moderate Alzheimer's Disease: The OmegAD Study. Journal of Alzheimer's Disease, 69(1), 189-197
Åpne denne publikasjonen i ny fane eller vindu >>Homocysteine Status Modifies the Treatment Effect of Omega-3 Fatty Acids on Cognition in a Randomized Clinical Trial in Mild to Moderate Alzheimer's Disease: The OmegAD Study
Vise andre…
2019 (engelsk)Inngår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 69, nr 1, s. 189-197Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Trials of supplementation with omega-3 fatty acids (omega 3-FAs) in patients with mild cognitive impairment or Alzheimer's disease (AD) have produced inconsistent effects on cognitive decline. There is evidence of an interaction between B vitamin status and omega 3-FAs in relation to brain atrophy and cognitive decline.

Objective: We investigated whether baseline levels of plasma total homocysteine (tHcy), a marker of B vitamin status, modify the effects of omega 3-FAs supplementation on cognitive performance in moderate AD.

Methods: This post hoc analysis of the OmegAD trial included 171 community-based patients with AD (MMSE >= 15): 88 patients received daily doses of 1.7 g docosahexaenoic acid and 0.6 g eicosapentaenoic acid for 6 months. Treatment outcome on cognition was analyzed according to baseline levels of tHcy using a general linear model and ANCOVA.

Results: We found significant interactions between omega 3-FA supplementation and tHcy on cognition and clinical stage assessed by MMSE (p = 0.040), global CDR (p = 0.059), and CDRsob (p = 0.023), but not on ADAS-cog (p = 0.649). In patients with tHcy levels <11.7 mu mol/L, omega 3-FA supplementation improved cognitive performance as measured by MMSE (+7.1%, 95% CI: 0.59 to 13.7%, p = 0.033) and clinical status as measured by CDRsob (-22.3%, 95% CI: -5.8 to -38.7%, p = 0.009) compared with placebo.

Conclusion: The effect of omega 3-FA supplementation on MMSE and CDR appears to be influenced by baseline tHcy, suggesting that adequate B vitamin status is required to obtain beneficial effects of omega 3-FA on cognition.

Emneord
Alzheimer's disease, B vitamins, cognition, dementia, homocysteine, omega-3 fatty acids
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-384475 (URN)10.3233/JAD-181148 (DOI)000467519100017 ()30958356 (PubMedID)
Forskningsfinansiär
The Swedish Brain FoundationThe Dementia Association - The National Association for the Rights of the DementedThe Karolinska Institutet's Research FoundationStiftelsen Gamla TjänarinnorÅke Wiberg Foundation, M16-0251Swedish Nutrition Foundation (SNF)Gun och Bertil Stohnes StiftelseSwedish Society of Medicine
Tilgjengelig fra: 2019-06-11 Laget: 2019-06-11 Sist oppdatert: 2019-06-11bibliografisk kontrollert
Faxen-Irving, G., Falahati, F., Basun, H., Eriksdotter, M., Vedin, I., Wahlund, L.-O., . . . Freund-Levi, Y. (2018). Does Fatty Acid Composition in Subcutaneous Adipose Tissue Differ between Patients with Alzheimer's Disease and Cohabiting Proxies?. Journal of Alzheimer's Disease, 61(2), 515-519
Åpne denne publikasjonen i ny fane eller vindu >>Does Fatty Acid Composition in Subcutaneous Adipose Tissue Differ between Patients with Alzheimer's Disease and Cohabiting Proxies?
Vise andre…
2018 (engelsk)Inngår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 61, nr 2, s. 515-519Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Low tissue levels of the major marine ω3 fatty acids (FAs) DHA and EPA are found in Alzheimer’s disease (AD). We investigated if healthy proxies to AD patients have higher levels of these ω3 FAs. We observed lower levels of EPA and DHA in subcutaneous adipose tissue biopsies from 64 AD patients compared with 16 cognitively healthy proxies. No significant difference was observed when pairwise comparisons were made between a subset of 16 AD patients and their co-habiting proxies. Larger studies are needed to replicate these findings and to determine if they could depend on FA intake or differences in metabolism.

Emneord
Alzheimer's disease, cognition, cohabitants, DHA, EPA, omega 3 fatty acids, subcutaneous adipose tissue
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-343881 (URN)10.3233/JAD-170359 (DOI)000422844100004 ()29154271 (PubMedID)
Forskningsfinansiär
Stockholm County CouncilStiftelsen Gamla TjänarinnorSwedish Society of MedicineThe Dementia Association - The National Association for the Rights of the Demented
Tilgjengelig fra: 2018-03-16 Laget: 2018-03-16 Sist oppdatert: 2018-03-16bibliografisk kontrollert
Abu Hamdeh, S., Rollman Waara, E., Möller, C., Söderberg, L., Basun, H., Alafuzoff, I., . . . Marklund, N. (2018). Rapid amyloid-β oligomer and protofibril accumulation in traumatic brain injury. Brain Pathology, 28(4), 451-462
Åpne denne publikasjonen i ny fane eller vindu >>Rapid amyloid-β oligomer and protofibril accumulation in traumatic brain injury
Vise andre…
2018 (engelsk)Inngår i: Brain Pathology, ISSN 1015-6305, E-ISSN 1750-3639, Vol. 28, nr 4, s. 451-462Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Deposition of amyloid-β (Aβ) is central to Alzheimer's disease (AD) pathogenesis and associated with progressive neurodegeneration in traumatic brain injury (TBI). We analyzed predisposing factors for Aβ deposition including monomeric Aβ40, Aβ42 and Aβ oligomers/protofibrils, Aβ species with pronounced neurotoxic properties, following human TBI. Highly selective ELISAs were used to analyze N-terminally intact and truncated Aβ40 and Aβ42, as well as Aβ oligomers/protofibrils, in human brain tissue, surgically resected from severe TBI patients (n = 12; mean age 49.5 ± 19 years) due to life-threatening brain swelling/hemorrhage within one week post-injury. The TBI tissues were compared to post-mortem AD brains (n = 5), to post-mortem tissue of neurologically intact (NI) subjects (n = 4) and to cortical biopsies obtained at surgery for idiopathic normal pressure hydrocephalus patients (iNPH; n = 4). The levels of Aβ40 and Aβ42 were not elevated by TBI. The levels of Aβ oligomers/protofibrils in TBI were similar to those in the significantly older AD patients and increased compared to NI and iNPH controls (P < 0.05). Moreover, TBI patients carrying the AD risk genotype Apolipoprotein E epsilon3/4 (APOE ε3/4; n = 4) had increased levels of Aβ oligomers/protofibrils (P < 0.05) and of both N-terminally intact and truncated Aβ42 (P < 0.05) compared to APOE ε3/4-negative TBI patients (n = 8). Neuropathological analysis showed insoluble Aβ aggregates (commonly referred to as Aβ plaques) in three TBI patients, all of whom were APOE ε3/4 carriers. We conclude that soluble intermediary Aβ aggregates form rapidly after TBI, especially among APOE ε3/4 carriers. Further research is needed to determine whether these aggregates aggravate the clinical short- and long-term outcome in TBI.

Emneord
Alzheimer's disease, amyloid β oligomers, amyloid-β, traumatic brain injury
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-341911 (URN)10.1111/bpa.12532 (DOI)000439749700001 ()28557010 (PubMedID)
Forskningsfinansiär
The Swedish Brain FoundationSwedish Research CouncilSwedish Institute
Merknad

De två första författarna delar förstaförfattarskapet.

Tilgjengelig fra: 2018-02-15 Laget: 2018-02-15 Sist oppdatert: 2019-07-03bibliografisk kontrollert
Karimi, M., Vedin, I., Levi, Y. F., Basun, H., Irving, G. F., Eriksdotter, M., . . . Palmblad, J. (2017). DHA-rich n-3 fatty acid supplementation decreases DNA methylation in blood leukocytes: the OmegAD study. American Journal of Clinical Nutrition, 106(4), 1157-1165
Åpne denne publikasjonen i ny fane eller vindu >>DHA-rich n-3 fatty acid supplementation decreases DNA methylation in blood leukocytes: the OmegAD study
Vise andre…
2017 (engelsk)Inngår i: American Journal of Clinical Nutrition, ISSN 0002-9165, E-ISSN 1938-3207, Vol. 106, nr 4, s. 1157-1165Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Dietary fish oils, rich in long-chain n-3 (omega-3) fatty acids (FAs) [e.g., docosahexaenoic acid (DHA, 22:6n-3) and eicosapentaenoic acid (EPA, 20:5n-3)], modulate inflammatory reactions through various mechanisms, including gene expression, which is measured as messenger RNA concentration. However, the effects of long-term treatment of humans with DHA and EPA on various epigenetic factors-such as DNA methylation, which controls messenger RNA generation-are poorly described. Objective: We wanted to determine the effects of 6 mo of dietary supplementation with an n-3 FA preparation rich in DHA on global DNA methylation of peripheral blood leukocytes (PBLs) and the relation to plasma EPA and DHA concentrations in Alzheimer disease (AD) patients. Design: In the present study, DNA methylation in four 5'-cytosinephosphate- guanine-3' (CpG) sites of long interspersed nuclear element-1 repetitive sequences was assessed in a group of 63 patients (30 given the n-3 FA preparation and 33 given placebo) as an estimation of the global DNA methylation in blood cells. Patients originated from the randomized, double-blind, placebo-controlled OmegAD study, in which 174 AD patients received either 1.7 g DHA and 0.6 g EPA (the n-3 FA group) or placebo daily for 6 mo. Results: At 6 mo, the n-3 FA group displayed marked increases in DHA and EPA plasma concentrations (2.6-and 3.5-fold), as well as decreased methylation in 2 out of 4 CpG sites (P<0.05 for all), respectively. This hypomethylation in CpG2 and CpG4 sites showed a reverse correlation to changes in plasma EPA concentration (r = -0.25, P = 0.045; and r = -0.26, P = 0.041, respectively), but not to changes in plasma DHA concentration, and were not related to apolipoprotein E-4 allele frequency. Conclusion: Supplementation with n-3 FA for 6 mo was associated with global DNA hypomethylation in PBLs. Our data may be of importance in measuring various effects of marine oils, including gene expression, in patients with AD and in other patients taking n-3 FA supplements. This trial was registered at clinicaltrials.gov as NCT00211159.

sted, utgiver, år, opplag, sider
AMER SOC NUTRITION-ASN, 2017
Emneord
fish oil, DHA, EPA, DNA methylation, LINE-1, Alzheimer disease
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-337084 (URN)10.3945/ajcn.117.155648 (DOI)000412004300022 ()28855224 (PubMedID)
Tilgjengelig fra: 2018-01-31 Laget: 2018-01-31 Sist oppdatert: 2018-02-22bibliografisk kontrollert
Almkvist, O., Rodriguez-Vieitez, E., Thordardottir, S., Amberla, K., Axelman, K., Basun, H., . . . Graff, C. (2017). Predicting Cognitive Decline across Four Decades in Mutation Carriers and Non-carriers in Autosomal-Dominant Alzheimer's Disease. Journal of the International Neuropsychological Society, 23(3), 195-203
Åpne denne publikasjonen i ny fane eller vindu >>Predicting Cognitive Decline across Four Decades in Mutation Carriers and Non-carriers in Autosomal-Dominant Alzheimer's Disease
Vise andre…
2017 (engelsk)Inngår i: Journal of the International Neuropsychological Society, ISSN 1355-6177, E-ISSN 1469-7661, Vol. 23, nr 3, s. 195-203Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objectives: The aim of this study was to investigate cognitive performance including preclinical and clinical disease course in carriers and non-carriers of autosomal-dominant Alzheimer's disease (adAD) in relation to multiple predictors, that is, linear and non-linear estimates of years to expected clinical onset of disease, years of education and age. Methods: Participants from five families with early-onset autosomal-dominant mutations (Swedish and Arctic APP, PSEN1 M146V, H163Y, and I143T) included 35 carriers (28 without dementia and 7 with) and 44 non-carriers. All participants underwent a comprehensive clinical evaluation, including neuropsychological assessment at the Memory Clinic, Karolinska University Hospital at Huddinge, Stockholm, Sweden. The time span of disease course covered four decades of the preclinical and clinical stages of dementia. Neuropsychological tests were used to assess premorbid and current global cognition, verbal and visuospatial functions, short-term and episodic memory, attention, and executive function. Results: In carriers, the time-related curvilinear trajectory of cognitive function across disease stages was best fitted to a formulae with three predictors: years to expected clinical onset (linear and curvilinear components), and years of education. In non-carriers, the change was minimal and best predicted by two predictors: education and age. The trajectories for carriers and non-carriers began to diverge approximately 10 years before the expected clinical onset in episodic memory, executive function, and visuospatial function. Conclusions: The curvilinear trajectory of cognitive functions across disease stages was mimicked by three predictors in carriers. In episodic memory, executive and visuospatial functions, the point of diverging trajectories occurred approximately 10 years ahead of the clinical onset compared to non-carriers.

sted, utgiver, år, opplag, sider
CAMBRIDGE UNIV PRESS, 2017
Emneord
Autosomal-dominant, Alzheimer's disease, Mutation carrier, Cognition, Predictors, Age of onset
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-320865 (URN)10.1017/S1355617716001028 (DOI)000398488800001 ()28079014 (PubMedID)
Forskningsfinansiär
The Swedish Brain FoundationThe Dementia Association - The National Association for the Rights of the DementedStockholm County CouncilSwedish Research CouncilThe Karolinska Institutet's Research Foundation
Tilgjengelig fra: 2017-04-26 Laget: 2017-04-26 Sist oppdatert: 2017-04-26bibliografisk kontrollert
Gunnarsson, M. D., Ingelsson, M., Blennow, K., Basun, H., Lannfelt, L. & Kilander, L. (2016). High tau levels in cerebrospinal fluid predict nursing home placement and rapid progression in Alzheimer's disease. Alzheimer's Research & Therapy, 8, Article ID 22.
Åpne denne publikasjonen i ny fane eller vindu >>High tau levels in cerebrospinal fluid predict nursing home placement and rapid progression in Alzheimer's disease
Vise andre…
2016 (engelsk)Inngår i: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 8, artikkel-id 22Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Increased concentrations of cerebrospinal fluid (CSF) total tau (t-tau) and phosphorylated tau, as well as decreased amyloid-beta 42 peptide, are biomarkers of Alzheimer's disease (AD) pathology, but few studies have shown an association with AD progression rate. We hypothesized that high CSF tau, as a marker of ongoing neurodegeneration, would predict a more aggressive course of AD, using time to nursing home placement (NHP) as the main outcome. Methods: Our sample inlcuded 234 patients with mild cognitive impairment (MCI) due to AD (n = 134) or mild to moderate AD (n = 100) who underwent lumbar puncture at a memory clinic and were followed for 2-11 years (median 4.9 years). Results: Individuals with CSF t-tau in the highest quartile (>= 900 ng/L) had a higher ratio of NHP, both in the total cohort and in patients with MCI only (adjusted HR 2.17 [95 % CI 1.24-3.80]; HR 2.37 [95 % CI 1.10-5.09], respectively), than the lowest quartile. The association between high t-tau levels and future steep deterioration was confirmed in analyses with conversion to moderate dementia (HR 1.66; 95 % CI 1.08-2.56), rapid decline in Mini Mental State Examination score (>= 4-point drop/12 months), and dying in severe dementia as outcomes. Conclusions: To our knowledge, this is the first study to show that high CSF t-tau levels predict early NHP and conversion to moderate dementia in an AD cohort. Selecting patients with high CSF t-tau, indicating more aggressive neurodegeneration and steeper decline, for AD immunotherapy trials might increase the possibility of showing contrast between active treatment and placebo.

Emneord
Nursing home placement, NHP, Alzheimer's disease, CSF, Tau, p-tau, Amyloid-beta, Rapid decline, Moderate dementia, Death in severe dementia
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-298845 (URN)10.1186/s13195-016-0191-0 (DOI)000376959600001 ()
Tilgjengelig fra: 2016-07-11 Laget: 2016-07-11 Sist oppdatert: 2019-05-09bibliografisk kontrollert
Logovinsky, V., Satlin, A., Lai, R., Swanson, C., Kaplow, J., Osswald, G., . . . Lannfelt, L. (2016). Safety and tolerability of BAN2401 - a clinical study in Alzheimer's disease with a protofibril selective A beta antibody. Alzheimer's Research & Therapy, 8, Article ID 14.
Åpne denne publikasjonen i ny fane eller vindu >>Safety and tolerability of BAN2401 - a clinical study in Alzheimer's disease with a protofibril selective A beta antibody
Vise andre…
2016 (engelsk)Inngår i: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 8, artikkel-id 14Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Several monoclonal antibodies for the treatment of Alzheimer's disease (AD) have been in development over the last decade. BAN2401 is a monoclonal antibody that selectively binds soluble amyloid beta (A beta) protofibrils.

Methods: Here we describe the first clinical study with BAN2401. Safety and tolerability were investigated in mild to moderate AD. A study design was used with staggered parallel single and multiple ascending doses, from 0.1 mg/kg as a single dose to 10 mg/kg biweekly for four months. The presence of amyloid related imaging abnormalities (ARIA, E for edema, H for hemorrhage) was assessed with magnetic resonance imaging (MRI). Cerebrospinal fluid (CSF) and plasma samples were analyzed to investigate pharmacokinetics (PK) and effects on biomarkers.

Results: The incidence of ARIA-E/H on MRI was comparable to that of placebo. BAN2401 exposure was approximately dose proportional, with a serum terminal elimination half-life of similar to 7 days. Only a slight increase of plasma A beta((1-40)) was observed but there were no measurable effects of BAN2401 on CSF biomarkers. On the basis of these findings Phase 2b efficacy study has been initiated in early AD.

Conclusions: BAN2401 was well-tolerated across all doses. The PK profile has guided us for selecting dose and dose regimens in the ongoing phase 2b study. There was no clear guidance for an effective dose based on biomarkers.

Emneord
Alzheimer's disease, Amyloid-beta, A beta, Protofibril, Immunotherapy, BAN2401, mAb158, ARIA, Clinical trial
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-294671 (URN)10.1186/s13195-016-0181-2 (DOI)000373482700001 ()27048170 (PubMedID)
Tilgjengelig fra: 2016-06-01 Laget: 2016-05-26 Sist oppdatert: 2019-05-09bibliografisk kontrollert
Matsunaga, S., Kishi, T., Annas, P., Basun, H., Hampel, H. & Iwata, N. (2015). Lithium as a Treatment for Alzheimer's Disease: A Systematic Review and Meta-Analysis. Journal of Alzheimer's Disease, 48(2), 403-410
Åpne denne publikasjonen i ny fane eller vindu >>Lithium as a Treatment for Alzheimer's Disease: A Systematic Review and Meta-Analysis
Vise andre…
2015 (engelsk)Inngår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 48, nr 2, s. 403-410Artikkel, forskningsoversikt (Fagfellevurdert) Published
Abstract [en]

Background: This is the first meta-analysis of randomized placebo-controlled trials testing lithium as a treatment for patients with Alzheimer's disease (AD) and individuals with mild cognitive impairment (MCI). Methods: The primary outcome measure was efficacy on cognitive performance as measured through the Alzheimer's Disease Assessment Scale cognitive subscale or the Mini-Mental State Examination. Other outcome measures were drug discontinuation rate, individual side effects, and biological markers (phosphorylated tau 181, total tau, and amyloid-beta(42)) in cerebrospinal fluid (CSF). Results: Three clinical trials including 232 participants that met the study's inclusion criteria were identified. Lithium significantly decreased cognitive decline as compared to placebo (standardized mean difference = -0.41, 95% confidence interval = -0.81 to -0.02, p = 0.04, I-2 = 47%, 3 studies, n = 199). There were no significant differences in the rate of attrition, discontinuation due to all causes or adverse events, or CSF biomarkers between treatment groups. Conclusions: The results indicate that lithium treatment may have beneficial effects on cognitive performance in subjects with MCI and AD dementia.

Emneord
Alzheimer's disease, lithium, meta-analysis, mild cognitive impairment, systematic review
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-265967 (URN)10.3233/JAD-150437 (DOI)000361066200009 ()26402004 (PubMedID)
Tilgjengelig fra: 2015-11-04 Laget: 2015-11-04 Sist oppdatert: 2018-01-10bibliografisk kontrollert
Eriksdotter, M., Vedin, I., Falahati, F., Freund-Levi, Y., Hjorth, E., Faxen-Irving, G., . . . Palmblad, J. (2015). Plasma Fatty Acid Profiles in Relation to Cognition and Gender in Alzheimer's Disease Patients During Oral Omega-3 Fatty Acid Supplementation: The OmegAD Study. Journal of Alzheimer's Disease, 48(3), 805-812
Åpne denne publikasjonen i ny fane eller vindu >>Plasma Fatty Acid Profiles in Relation to Cognition and Gender in Alzheimer's Disease Patients During Oral Omega-3 Fatty Acid Supplementation: The OmegAD Study
Vise andre…
2015 (engelsk)Inngår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 48, nr 3, s. 805-812Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: omega 3 fatty acids (omega 3 FAs) may slow the rate of decline in cognitive performance in mild forms of cognitive impairment and Alzheimer's disease (AD). However, the relationship between changes of plasma omega 3 FA levels and cognitive performance, as well as effects of gender, are poorly known. Objective: To study the effect of 6-month administration of DHA-rich omega 3 FA supplementation on plasma FA profiles in patients with mild to moderate AD in relation to cognitive performance and gender. This investigation is part of the OmegAD Study. Methods: 174 AD patients (74 +/- 9 years) were randomized to a daily intake of 2.3g omega 3 FA or placebo for 6 months; subsequently all received the omega 3 FA preparation for the next 6 months. Baseline as well as changes in plasma levels of the main omega 3 FAs in 165 patients, while receiving omega 3 FA supplementation for 6 months, were analyzed for association to cognitive performance (assessed by ADAS-cog and MMSE scores) as well as to gender. Results: Preservation of cognitive functioning, assessed by ADAS-cog or its sub-items (but not MMSE) scores, was significantly associated to increasing plasma omega 3 FA levels over time. Thus, the higher omega 3 FA plasma levels rose, the lower was the rate of cognitive deterioration. This effect was not related to gender; since although females displayed higher omega 3 FA plasma levels than did males after 6 months of supplementation, this difference disappeared when adjusted for body weight. Conclusions: Since our study suggests dose-response relationships between plasma levels of omega 3 FA and preservation of cognition, future omega 3 FA trials in patients with mild AD should consider exploring graded (and body weight adjusted) doses of omega 3 FA.

Emneord
Alzheimer's disease, cognition, DHA, EPA, gender, omega 3 fatty acids
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-267086 (URN)10.3233/JAD-150102 (DOI)000362958800022 ()26402079 (PubMedID)
Forskningsfinansiär
Stockholm County Council
Tilgjengelig fra: 2015-11-20 Laget: 2015-11-17 Sist oppdatert: 2018-02-22
Freund-Levi, Y., Vedin, I., Hjorth, E., Basun, H., Irving, G. F., Schultzberg, M., . . . Basu, S. (2014). Effects of Supplementation with Omega-3 Fatty Acids on Oxidative Stress and Inflammation in Patients with Alzheimer's Disease: The OmegAD Study. Journal of Alzheimer's Disease, 42(3), 823-831
Åpne denne publikasjonen i ny fane eller vindu >>Effects of Supplementation with Omega-3 Fatty Acids on Oxidative Stress and Inflammation in Patients with Alzheimer's Disease: The OmegAD Study
Vise andre…
2014 (engelsk)Inngår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 42, nr 3, s. 823-831Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Oxidative stress and inflammation are two key mechanisms suggested to be involved in the pathogenesis of Alzheimer's disease (AD). Omega-3 fatty acids (omega-3 FAs) found in fish and fish oil have several biological properties that may be beneficial in AD. However, they may also auto-oxidize and induce in vivo lipid peroxidation. Objective: The objective of this study was to evaluate systemic oxidative stress and inflammatory biomarkers following oral supplementation of dietary omega-3 FA. Methods: Forty patients with moderate AD were randomized to receive 1.7 g DHA (22:6) and 0.6 g EPA (20:5) or placebo for 6 months. Urinary samples were collected before and after supplementation. The levels of the major F-2-isoprostane, 8-iso-PGF(2 alpha) a consistent in vivo biomarker of oxidative stress, and 15-keto-dihydro-PGF(2 alpha), a major metabolite of PGF(2 alpha) and biomarker of inflammatory response, were measured. Results: F-2-isoprostane in urine increased in the placebo group after 6 months, but therewas no clear difference in treatment effect between supplemented and non-supplemented patients on the urinary levels of F-2-isoprostanes and 15-keto-dihydro-PGF(2 alpha). At baseline, the levels of 15-keto-dihydro-PGF(2 alpha) showed negative correlative relationships to omega-3 FAs, and a positive correlation to linoleic acid. 8-iso-PGF(2 alpha) correlated negatively to the omega-6 FA arachidonic acid. Conclusion: The findings indicate that supplementation of omega-3 FAs to patients with AD for 6 months does not have a clear effect on free radical-mediated formation of F-2-isoprostane or cyclooxygenase-mediated formation of prostaglandin F-2 alpha. The correlative relationships to FAs indicate a potential role of FAs in immunoregulation.

Emneord
Alzheimer's disease, eicosanoids, F-2-isoprostane, inflammation, lipids, omega-3 fatty acids, oxidative stress, prostaglandin F-2 alpha
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-235525 (URN)10.3233/JAD-132042 (DOI)000342237000011 ()
Tilgjengelig fra: 2014-11-05 Laget: 2014-11-05 Sist oppdatert: 2018-02-22bibliografisk kontrollert
Organisasjoner