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Sökning: WFRF:(Grenier Beatrice)

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1.
  • Faure, Quentin, et al. (författare)
  • Tomonaga-Luttinger Liquid Spin Dynamics in the Quasi-One-Dimensional Ising-Like Antiferromagnet BaCo2V2O8
  • 2019
  • Ingår i: Physical Review Letters. - : American Physical Society. - 0031-9007 .- 1079-7114. ; 123:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Combining inelastic neutron scattering and numerical simulations, we study the quasi-one-dimensional Ising anisotropic quantum antiferromagnet BaCo2V2O8 in a longitudinal magnetic field. This material shows a quantum phase transition from a Neel ordered phase at zero field to a longitudinal incommensurate spin density wave at a critical magnetic field of 3.8 T. Concomitantly, the excitation gap almost closes and a fundamental reconfiguration of the spin dynamics occurs. These experimental results are well described by the universal Tomonaga-Luttinger liquid theory developed for interacting spinless fermions in one dimension. We especially observe the rise of mainly longitudinal excitations, a hallmark of the unconventional low-field regime in Ising-like quantum antiferromagnetic chains.
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2.
  • Faure, Quentin, et al. (författare)
  • Topological quantum phase transition in the Ising-like antiferromagnetic spin chain BaCo2V2O8
  • 2018
  • Ingår i: Nature Physics. - : Nature Publishing Group. - 1745-2473 .- 1745-2481. ; 14:7, s. 716-722
  • Tidskriftsartikel (refereegranskat)abstract
    • Since the seminal ideas of Berezinskii, Kosterlitz and Thouless, topological excitations have been at the heart of our understanding of a whole novel class of phase transitions. In most cases, those transitions are controlled by a single type of topological objects. There are, however, some situations, still poorly understood, where two dual topological excitations fight to control the phase diagram and the transition. Finding experimental realizations of such cases is thus of considerable interest. We show here that this situation occurs in BaCo2V2O8, a spin-1/2 Ising-like quasi-one-dimensional antiferromagnet, when subjected to a uniform magnetic field transverse to the Ising axis. Using neutron scattering experiments, we measure a drastic modification of the quantum excitations beyond a critical value of the magnetic field. This quantum phase transition is identified, through a comparison with theoretical calculations, to be a transition between two different types of solitonic topological object, which are captured by different components of the dynamical structure factor.
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3.
  • Le Guen, Yann, et al. (författare)
  • Multiancestry analysis of the HLA locus in Alzheimer's and Parkinson's diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes.
  • 2023
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences (PNAS). - 1091-6490 .- 0027-8424. ; 120:36
  • Tidskriftsartikel (refereegranskat)abstract
    • Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson's disease (PD) and Alzheimer's disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1*04:07, and intermediary with HLA-DRB1*04:01 and HLA-DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased Aβ42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues.
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4.
  • Luo, Jiao, et al. (författare)
  • Genetic Associations Between Modifiable Risk Factors and Alzheimer Disease
  • 2023
  • Ingår i: JAMA Network Open. - : American Medical Association (AMA). - 2574-3805. ; 6:5
  • Tidskriftsartikel (refereegranskat)abstract
    • IMPORTANCE An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course. However, robust evidence for most of these risk factors is lacking. Effective interventions should target risk factors in the causal pathway to dementia.OBJECTIVE To comprehensively disentangle potentially causal aspects of modifiable risk factors for Alzheimer disease (AD) to inspire new drug targeting and improved prevention.DESIGN, SETTING, AND PARTICIPANTS This genetic association study was conducted using 2-sample univariable and multivariable mendelian randomization. Independent genetic variants associated with modifiable risk factors were selected as instrumental variables from genomic consortia. Outcome data for AD were obtained from the European Alzheimer & Dementia Biobank (EADB), generated on August 31, 2021. Main analyses were conducted using the EADB clinically diagnosed end point data. All analyses were performed between April 12 and October 27, 2022.EXPOSURES Genetically determined modifiable risk factors. MAIN OUTCOMES AND MEASURES Odds ratios (ORs) and 95% CIs for AD were calculated per 1-unit change of genetically determined risk factors.RESULTS The EADB-diagnosed cohort included 39106 participants with clinically diagnosed AD and 401577 control participants without AD. The mean age ranged from 72 to 83 years for participants with AD and 51 to 80 years for control participants. Among participants with AD, 54% to 75% were female, and among control participants, 48% to 60% were female. Genetically determined high-density lipoprotein (HDL) cholesterol concentrations were associated with increased odds of AD (OR per 1-SD increase, 1.10 [95% CI, 1.05-1.16]). Genetically determined high systolic blood pressure was associated with increased risk of AD after adjusting for diastolic blood pressure (OR per 10-mm Hg increase, 1.22 [95% CI, 1.02-1.46]). In a second analysis to minimize bias due to sample overlap, the entire UK Biobank was excluded from the EADB consortium; odds for AD were similar for HDL cholesterol (OR per 1-SD unit increase, 1.08 [95% CI, 1.02-1.15]) and systolic blood pressure after adjusting for diastolic blood pressure (OR per 10-mm Hg increase, 1.23 [95% CI, 1.01-1.50]).CONCLUSIONS AND RELEVANCE This genetic association study found novel genetic associations between high HDL cholesterol concentrations and high systolic blood pressure with higher risk of AD. These findings may inspire new drug targeting and improved prevention implementation.
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