SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Camus M) "

Sökning: WFRF:(Camus M)

  • Resultat 1-10 av 19
  • [1]2Nästa
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Mattsson, Niklas, et al. (författare)
  • Prevalence of the apolipoprotein E ε4 allele in amyloid β positive subjects across the spectrum of Alzheimer's disease
  • 2018
  • Ingår i: Alzheimer's and Dementia. - : Wiley. - 1552-5260 .- 1552-5279. ; 14:7, s. 913-924
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Apolipoprotein E (APOE) ε4 is the major genetic risk factor for Alzheimer's disease (AD), but its prevalence is unclear because earlier studies did not require biomarker evidence of amyloid β (Aβ) pathology. Methods: We included 3451 Aβ+ subjects (853 AD-type dementia, 1810 mild cognitive impairment, and 788 cognitively normal). Generalized estimating equation models were used to assess APOE ε4 prevalence in relation to age, sex, education, and geographical location. Results: The APOE ε4 prevalence was 66% in AD-type dementia, 64% in mild cognitive impairment, and 51% in cognitively normal, and it decreased with advancing age in Aβ+ cognitively normal and Aβ+ mild cognitive impairment (P <.05) but not in Aβ+ AD dementia (P =.66). The prevalence was highest in Northern Europe but did not vary by sex or education. Discussion: The APOE ε4 prevalence in AD was higher than that in previous studies, which did not require presence of Aβ pathology. Furthermore, our results highlight disease heterogeneity related to age and geographical location.
  •  
2.
  • Jansen, Willemijn J, et al. (författare)
  • Association of Cerebral Amyloid-β Aggregation With Cognitive Functioning in Persons Without Dementia.
  • 2018
  • Ingår i: JAMA psychiatry. - : American Medical Association. - 2168-6238 .- 2168-622X. ; 75:1, s. 84-95
  • Tidskriftsartikel (refereegranskat)abstract
    • Cerebral amyloid-β aggregation is an early event in Alzheimer disease (AD). Understanding the association between amyloid aggregation and cognitive manifestation in persons without dementia is important for a better understanding of the course of AD and for the design of prevention trials.To investigate whether amyloid-β aggregation is associated with cognitive functioning in persons without dementia.This cross-sectional study included 2908 participants with normal cognition and 4133 with mild cognitive impairment (MCI) from 53 studies in the multicenter Amyloid Biomarker Study. Normal cognition was defined as having no cognitive concerns for which medical help was sought and scores within the normal range on cognitive tests. Mild cognitive impairment was diagnosed according to published criteria. Study inclusion began in 2013 and is ongoing. Data analysis was performed in January 2017.Global cognitive performance as assessed by the Mini-Mental State Examination (MMSE) and episodic memory performance as assessed by a verbal word learning test. Amyloid aggregation was measured with positron emission tomography or cerebrospinal fluid biomarkers and dichotomized as negative (normal) or positive (abnormal) according to study-specific cutoffs. Generalized estimating equations were used to examine the association between amyloid aggregation and low cognitive scores (MMSE score ≤27 or memory z score≤-1.28) and to assess whether this association was moderated by age, sex, educational level, or apolipoprotein E genotype.Among 2908 persons with normal cognition (mean [SD] age, 67.4 [12.8] years), amyloid positivity was associated with low memory scores after age 70 years (mean difference in amyloid positive vs negative, 4% [95% CI, 0%-7%] at 72 years and 21% [95% CI, 10%-33%] at 90 years) but was not associated with low MMSE scores (mean difference, 3% [95% CI, -1% to 6%], P = .16). Among 4133 patients with MCI (mean [SD] age, 70.2 [8.5] years), amyloid positivity was associated with low memory (mean difference, 16% [95% CI, 12%-20%], P < .001) and low MMSE (mean difference, 14% [95% CI, 12%-17%], P < .001) scores, and this association decreased with age. Low cognitive scores had limited utility for screening of amyloid positivity in persons with normal cognition and those with MCI. In persons with normal cognition, the age-related increase in low memory score paralleled the age-related increase in amyloid positivity with an intervening period of 10 to 15 years.Although low memory scores are an early marker of amyloid positivity, their value as a screening measure for early AD among persons without dementia is limited.
  •  
3.
  • Vermunt, L., et al. (författare)
  • Duration of preclinical, prodromal, and dementia stages of Alzheimer's disease in relation to age, sex, and APOE genotype
  • 2019
  • Ingår i: Alzheimers & Dementia. - : Elsevier. - 1552-5260 .- 1552-5279. ; 15:7, s. 888-898
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: We estimated the age-specific duration of the preclinical, prodromal, and dementia stages of Alzheimer's disease (AD) and the influence of sex, setting, apolipoprotein E (APOE) genotype, and cerebrospinal fluid tau on disease duration. Methods: We performed multistate modeling in a combined sample of 6 cohorts (n = 3268) with death as the end stage and estimated the preclinical, prodromal, and dementia stage duration. Results: The overall AD duration varied between 24 years (age 60) and 15 years (age 80). For individuals presenting with preclinical AD, age 70, the estimated preclinical AD duration was 10 years, prodromal AD 4 years, and dementia 6 years. Male sex, clinical setting, APOE epsilon 4 allele carriership, and abnormal cerebrospinal fluid tau were associated with a shorter duration, and these effects depended on disease stage. Discussion: Estimates of AD disease duration become more accurate if age, sex, setting, APOE, and cerebrospinal fluid tau are taken into account. This will be relevant for clinical practice and trial design. (C) 2019 the Alzheimer's Association. Published by Elsevier Inc. All rights reserved.
  •  
4.
  • Vieira-Silva, S., et al. (författare)
  • Statin therapy is associated with lower prevalence of gut microbiota dysbiosis
  • 2020
  • Ingår i: Nature. - 0028-0836 .- 1476-4687. ; 581:7808, s. 310-315
  • Tidskriftsartikel (refereegranskat)abstract
    • Microbiome community typing analyses have recently identified the Bacteroides2 (Bact2) enterotype, an intestinal microbiota configuration that is associated with systemic inflammation and has a high prevalence in loose stools in humans1,2. Bact2 is characterized by a high proportion of Bacteroides, a low proportion of Faecalibacterium and low microbial cell densities1,2, and its prevalence varies from 13% in a general population cohort to as high as 78% in patients with inflammatory bowel disease2. Reported changes in stool consistency3 and inflammation status4 during the progression towards obesity and metabolic comorbidities led us to propose that these developments might similarly correlate with an increased prevalence of the potentially dysbiotic Bact2 enterotype. Here, by exploring obesity-associated microbiota alterations in the quantitative faecal metagenomes of the cross-sectional MetaCardis Body Mass Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversification. By focusing on a subcohort of participants that are not medicated with statins, we find that the prevalence of Bact2 correlates with body mass index, increasing from 3.90% in lean or overweight participants to 17.73% in obese participants. Systemic inflammation levels in Bact2-enterotyped individuals are higher than predicted on the basis of their obesity status, indicative of Bact2 as a dysbiotic microbiome constellation. We also observe that obesity-associated microbiota dysbiosis is negatively associated with statin treatment, resulting in a lower Bact2 prevalence of 5.88% in statin-medicated obese participants. This finding is validated in both the accompanying MetaCardis cardiovascular disease dataset (n = 282) and the independent Flemish Gut Flora Project population cohort (n = 2,345). The potential benefits of statins in this context will require further evaluation in a prospective clinical trial to ascertain whether the effect is reproducible in a randomized population and before considering their application as microbiota-modulating therapeutics. © 2020, The Author(s), under exclusive licence to Springer Nature Limited.
  •  
5.
  • Jansen, Willemijn J, et al. (författare)
  • Prevalence of cerebral amyloid pathology in persons without dementia: a meta-analysis.
  • 2015
  • Ingår i: JAMA. - : American Medical Association. - 1538-3598 .- 0098-7484. ; 313:19, s. 1924-38
  • Tidskriftsartikel (refereegranskat)abstract
    • Cerebral amyloid-β aggregation is an early pathological event in Alzheimer disease (AD), starting decades before dementia onset. Estimates of the prevalence of amyloid pathology in persons without dementia are needed to understand the development of AD and to design prevention studies.
  •  
6.
  • Mattsson, Niklas, et al. (författare)
  • Prevalence of the apolipoprotein E epsilon 4 allele in amyloid beta positive subjects across the spectrum of Alzheimers disease
  • 2018
  • Ingår i: Alzheimer's & Dementia. - : ELSEVIER SCIENCE INC. - 1552-5260 .- 1552-5279. ; 14:7, s. 913-924
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Apolipoprotein E (APOE) epsilon 4 is the major genetic risk factor for Alzheimers disease (AD), but its prevalence is unclear because earlier studies did not require biomarker evidence of amyloid beta(A beta) pathology. Methods: We included 3451 A beta+ subjects (853 AD-type dementia, 1810 mild cognitive impairment, and 788 cognitively normal). Generalized estimating equation models were used to assess APOE epsilon 4 prevalence in relation to age, sex, education, and geographical location. Results: The APOE epsilon 4 prevalence was 66% in AD-type dementia, 64% in mild cognitive impairment, and 51% in cognitively normal, and it decreased with advancing age in A beta+ cognitively normal and A beta+ mild cognitive impairment (P amp;lt;.05) but not in A beta+ AD dementia (P =.66). The prevalence was highest in Northern Europe but did not vary by sex or education. Discussion: The APOE E4 prevalence in AD was higher than that in previous studies, which did not require presence of A beta pathology. Furthermore, our results highlight disease heterogeneity related to age and geographical location. (C) 2018 the Alzheimers Association. Published by Elsevier Inc. All rights reserved.
  •  
7.
  • Mendez-Hernandez, H., et al. (författare)
  • VALES VI: ISM enrichment in star-forming galaxies up to z similar to 0.2 using (CO)-C-12(1-0), (CO)-C-13(1-0), and (CO)-O-18(1-0) line luminosity ratios
  • 2020
  • Ingår i: Monthly Notices of the Royal Astronomical Society. - 0035-8711 .- 1365-2966. ; 497:3, s. 2771-2785
  • Tidskriftsartikel (refereegranskat)abstract
    • We present Atacama Large Millimeter/sub-millimeter Array (ALMA) observations towards 27 low-redshift (0.02< z< 0.2) starforming galaxies taken from the Valpara ' iso ALMA/APEX Line Emission Survey. We perform stacking analyses of the (CO)-C-12(1-0), (CO)-C-13(1-0), and (CO)-O-18(1-0) emission lines to explore the L' [(CO)-C-12(1-0)]/L' [(CO)-C-13(1-0)] [hereafter L' ((CO)-C-12)/L' ((CO)-C-13)] and L' [(CO)-C-13(1-0)]/L' [(CO)-O-18(1-0)] [hereafter L' ((CO)-C-13)/L' ((CO)-O-18)] line luminosity ratio dependence as a function of different global galaxy parameters related to the star formation activity. The sample has far-IR luminosities of 1010.1-11.9 L and stellar masses of 109.8-10.9M(circle dot) corresponding to typical star-forming and starburst galaxies at these redshifts. On average, we find an L' (12CO)/L' ((CO)-C-13) line luminosity ratio value of 16.1 +/- 2.5. Galaxies with pieces of evidence of possible merging activity tend to show higher L' ((CO)-C-12)/L' (13CO) ratios by a factor of 2, while variations of this order are also found in galaxy samples with higher star formation rates (SFRs) or star formation efficiencies (SFEs). We also find an average L' ((CO)-C-13)/L' ((CO)-O-18) line luminosity ratio of 2.5 +/- 0.6, which is in good agreement with those previously reported for starburst galaxies. We find that galaxy samples with high LIR, SFR, and SFE show low L' ((CO)-C-13)/L' ((CO)-O-18) line luminosity ratios with high L' ((CO)-C-12)/L' ((CO)-C-13) line luminosity ratios, suggesting that these trends are produced by selective enrichment of massive stars in young starbursts.
  •  
8.
  •  
9.
  • Molinaro, Antonio, et al. (författare)
  • Imidazole propionate is increased in diabetes and associated with dietary patterns and altered microbial ecology
  • 2020
  • Ingår i: Nature Communications. - 2041-1723. ; 11:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Microbiota-host-diet interactions contribute to the development of metabolic diseases. Imidazole propionate is a novel microbially produced metabolite from histidine, which impairs glucose metabolism. Here, we show that subjects with prediabetes and diabetes in the MetaCardis cohort from three European countries have elevated serum imidazole propionate levels. Furthermore, imidazole propionate levels were increased in subjects with low bacterial gene richness and Bacteroides 2 enterotype, which have previously been associated with obesity. The Bacteroides 2 enterotype was also associated with increased abundance of the genes involved in imidazole propionate biosynthesis from dietary histidine. Since patients and controls did not differ in their histidine dietary intake, the elevated levels of imidazole propionate in type 2 diabetes likely reflects altered microbial metabolism of histidine, rather than histidine intake per se. Thus the microbiota may contribute to type 2 diabetes by generating imidazole propionate that can modulate host inflammation and metabolism.
  •  
10.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 19
  • [1]2Nästa
Typ av publikation
tidskriftsartikel (19)
Typ av innehåll
refereegranskat (19)
Författare/redaktör
van der Flier, Wiesj ... (7)
Jansen, Willemijn J. (7)
Scheltens, P (6)
Rinne, Juha O. (6)
Frisoni, Giovanni B. (6)
Verbeek, Marcel M (6)
visa fler...
Rabinovici, Gil D (6)
Rowe, Christopher C (6)
Visser, Pieter Jelle (6)
Fagan, Anne M (6)
Tsolaki, Magda (5)
Tsolaki, M (5)
Jagust, William J. (5)
Scheltens, Philip (5)
Teunissen, Charlotte ... (5)
Villemagne, Victor L (5)
Cohen, Ann D (5)
Roe, Catherine M (5)
Vos, Stephanie J. B. (5)
Aarsland, Dag (4)
Van Laere, Koen (4)
Vandenberghe, Rik (4)
Marcusson, Jan (4)
Soininen, Hilkka (4)
Visser, PJ (4)
Alcolea, Daniel (4)
Fortea, Juan (4)
Lleó, Alberto (4)
Molinuevo, José Luis (4)
Kornhuber, Johannes (4)
Nordberg, Agneta (4)
Ossenkoppele, Rik (4)
Grimmer, Timo (4)
Drzezga, Alexander (4)
Fladby, Tormod (4)
van Waalwijk van Doo ... (4)
Engelborghs, Sebasti ... (4)
Mroczko, Barbara (4)
Waldemar, Gunhild (4)
Rami, Lorena (4)
Chen, Kewei (4)
Peters, Oliver (4)
Wiltfang, Jens (4)
Maier, Wolfgang (4)
Cavedo, Enrica (4)
Hampel, Harald (4)
Verhey, FRJ (4)
Freund-Levi, Yvonne (4)
Santana, Isabel (4)
Sarazin, Marie (4)
visa färre...
Lärosäte
Göteborgs universitet (6)
Uppsala universitet (4)
Örebro universitet (3)
Lunds universitet (3)
Chalmers tekniska högskola (3)
Karolinska Institutet (3)
visa fler...
Umeå universitet (2)
Linköpings universitet (1)
visa färre...
Språk
Engelska (19)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (10)
Naturvetenskap (3)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy