Anomalous spin-charge separation in a driven Hubbard system

Spin-charge separation (SCS) is a striking manifestation of strong correlations in low-dimensional quantum systems, whereby a fermion splits into separate spin and charge excitations that travel at different speeds. Here, we demonstrate that periodic driving enables control over SCS in a Hubbard system near half-filling. In one dimension, we predict analytically an exotic regime where charge travels slower than spin and can even become 'frozen', in agreement with numerical calculations. In two dimensions, the driving slows both charge and spin, and leads to complex interferences between single-particle and pair-hopping processes.Comment: arXiv admin note: text overlap with arXiv:2002.0231

Mott polaritons in cavity-coupled quantum materials

We show that strong electron-electron interactions in cavity-coupled quantum materials can enable collectively enhanced light-matter interactions with ultrastrong effective coupling strengths. As a paradigmatic example we consider a Fermi-Hubbard model coupled to a single-mode cavity and find that resonant electron-cavity interactions result in the formation of a quasi-continuum of polariton branches. The vacuum Rabi splitting of the two outermost branches is collectively enhanced and scales with $g_{\text{eff}}\propto\sqrt{2L}$, where $L$ is the number of electronic sites, and the maximal achievable value for $g_{\text{eff}}$ is determined by the volume of the unit cell of the crystal. We find that $g_{\text{eff}}$ for existing quantum materials can by far exceed the width of the first excited Hubbard band. This effect can be experimentally observed via measurements of the optical conductivity and does not require ultra-strong coupling on the single-electron level. Quantum correlations in the electronic ground state as well as the microscopic nature of the light-matter interaction enhance the collective light-matter interaction compared to an ensemble of independent two-level atoms interacting with a cavity mode.Comment: 11 pages, 4 figures. arXiv admin note: text overlap with arXiv:1806.0675

Controlling magnetic correlations in a driven Hubbard system far from half-filling

We propose using ultracold fermionic atoms trapped in a periodically shaken optical lattice as a quantum simulator of the t-J Hamiltonian, which describes the dynamics in doped antiferromagnets and is thought to be relevant to the problem of high-temperature superconductivity in the cuprates. We show analytically that the effective Hamiltonian describing this system for off-resonant driving is the t-J model with additional pair hopping terms, whose parameters can all be controlled by the drive. We then demonstrate numerically using tensor network methods for a 1D lattice that a slow modification of the driving strength allows near-adiabatic transfer of the system from the ground state of the underlying Hubbard model to the ground state of the effective t-J Hamiltonian. Finally, we report exact diagonalization calculations illustrating the control achievable on the dynamics of spin-singlet pairs in 2D lattices utilising this technique with current cold-atom quantum-simulation technology. These results open new routes to explore the interplay between density and spin in strongly-correlated fermionic systems through their out-of-equilibrium dynamics

Sense about science - making sense of crime

Booklet 'Making Sense of Crime' published by registered charity 'Sense About Science'There’s always heated debate about crime in the media and a lot of political argument about how we should respond to it. But these arguments rarely provide insight into what actually causes crime, what lies behind trends over time and in different places, and how best to go about reducing it. Values inform how a society decides to deal with crime. We may decide that rehabilitation is a better principle than punishment, and this will influence how we decide what is most effective. However, we also expect these choices to be disciplined by sound evidence, because if crime policy ignores what works and what doesn’t, there are likely to be bad social consequences. And with over £10bn spent annually on tackling crime through the police, prisons, probation and courts, unless we look at evidence we can’t see how effective any of it is. Crime policy usually has twin aims – to prevent crime, and to seek justice by punishing those who commit offences. Research shows there’s only a loose link, if any, between the way offenders are punished and the number of offences committed. There is no reliable evidence for example, that capital punishment reduces serious crimes as its supporters claim. Yet politicians and commentators regularly claim that more punishments are a way to cut crime. Academic, government and community organisations have all said crime policies need to be based more on evidence, but much of the evidence available at the moment is poor or unclear. Debates about crime rarely reflect how strong the evidence behind opposing policies is, and even when politicians honestly believe they’re following the evidence, they tend to select evidence that supports their political views. This guide looks at some of the key things we do know and why it has been so difficult to make sense of crime policy. An important point throughout is that policymakers sometimes have to make decisions when things are not clear-cut. They have a better chance of making effective policies if they admit to this uncertainty – and conduct robust research to find out more. In the following pages we have shared insights from experts in violent crime, policing, crime science, psychology and the media’s influence on the crime debate. They don’t have all the answers, but we hope they leave you better-placed to hold policymakers and commentators to account and promote a more useful discussion about crime

APOE ε4, Alzheimer's disease neuropathology, and sleep disturbance, in individuals with and without dementia

BACKGROUND: Apolipoprotein E epsilon 4 (APOE-ε4) carrier status is an established risk factor for Alzheimer’s disease (AD) dementia. It has also been linked with sleep disturbance in healthy older adults and increased insomnia risk. This association may be driven by the effect of APOE-ε4 on AD pathological change, itself associated with sleep abnormalities. To assess this relationship, we have evaluated post-mortem neuropathological findings in patients with and without cognitive impairment and AD pathology, who had extensive clinical assessment within 12 months of death. METHODS: This retrospective cohort study used UK Brain Banks Network data. Eligible subjects were aged over 50, with pre-mortem neuropsychiatry inventory scores of sleep disturbance (NPI-K), neurocognitive testing and functional cognitive status assessment (Clinical Dementia Rating scale). Neuropathological data included Thal phase, Braak stage and CERAD scores (measures of Aβ plaque distribution, tangle distribution and neuritic plaque density, respectively) combined to form the National Institute on Aging Alzheimer’s Association (NIA-AA) ABC score reflecting AD neuropathology. Participants with other significant intracerebral pathology or pathological features of non-AD dementia were excluded. Multivariate linear regression was performed with NPIK Global Score (NPIK frequency score multiplied by severity score) as the dependent variable and APOE-ε4 heterozygosity or homozygosity as independent variables. Covariates included age, gender, APOE-ε2 status and ABC NPI measures reflecting depression and anxiety. Further models stratified by ABC score and functional cognitive status were also produced. RESULTS: Seven hundred twenty-eight records were identified. Two hundred two participants were included in the final analysis: mean (SD) age 84.0 (9.2) and MMSE 14.0 (11.8). Mean sleep disturbance scores were highest in ε4 homozygosity (n=11), 4.55 (5.4); intermediate in ε4 heterozygosity (n=95), 2.03 (4.0); and lowest in non-ε4 carriers (n=96), 1.36 (3.3). Within the full sample, controlling for pathological status, age, gender, depression, anxiety and CDR-SOB status, APOE-ε4 homozygosity was associated with sleep disturbance (β 2.53, p=0.034). APOE-ε4 heterozygosity was similarly associated in individuals without dementia (β 1.21, p=0.048). CONCLUSION: These findings lend weight to the hypothesis that APOE-ε4 affects sleep by mechanisms independent of AD pathological change. Evaluation of those mechanisms would enhance understanding of sleep disturbance pathways and potentially provide treatment targets. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13195-022-00992-y

The Past, Present and Future of Sleep Measurement in Mild Cognitive Impairment and Early Dementia – Towards a Core Outcome Set:A Scoping Review

STUDY OBJECTIVES: Sleep abnormalities emerge early in dementia and may accelerate cognitive decline. Their accurate characterization may facilitate earlier clinical identification of dementia and allow for assessment of sleep intervention efficacy. This scoping review determines how sleep is currently measured and reported in Mild Cognitive Impairment (MCI) and early dementia, as a basis for future core outcome alignment. METHODS: This review follows the PRISMA Guidelines for Scoping Reviews. CINAHL, Embase, Medline, Psychinfo, and British Nursing Index databases were searched from inception—March 12, 2021. Included studies had participants diagnosed with MCI and early dementia and reported on sleep as a key objective/ outcome measure. RESULTS: Nineteen thousand five hundred and ninety-six titles were returned following duplicate removal with 188 studies [N] included in final analysis. Sleep data was reported on 17 139 unique, diagnostically diverse participants (n). “Unspecified MCI” was the most common diagnosis amongst patients with MCI (n = 5003, 60.6%). Despite technological advances, sleep was measured most commonly by validated questionnaires (n = 12 586, N = 131). Fewer participants underwent polysomnography (PSG) (n = 3492, N = 88) and actigraphy (n = 3359, N = 38) with little adoption of non-PSG electroencephalograms (EEG) (n = 74, N = 3). Sleep outcome parameters were reported heterogeneously. 62/165 (37.6%) were described only once in the literature (33/60 (60%) in interventional studies). There was underrepresentation of circadian (n = 725, N = 25) and micro-architectural (n = 360, N = 12) sleep parameters. CONCLUSIONS: Alongside under-researched areas, there is a need for more detailed diagnostic characterization. Due to outcome heterogeneity, we advocate for international consensus on core sleep outcome parameters to support causal inference and comparison of therapeutic sleep interventions

Cross-sectional and longitudinal association of sleep and Alzheimer biomarkers in cognitively unimpaired adults

Sleep abnormalities are prevalent in Alzheimer's disease, with sleep quality already impaired at its preclinical stage. Epidemiological and experimental data point to sleep abnormalities contributing to the risk of Alzheimer's disease. However, previous studies are limited by either a lack of Alzheimer's disease biomarkers, reduced sample size or cross-sectional design. Understanding if, when, and how poor sleep contributes to Alzheimer's disease progression is important so that therapies can be targeted to the right phase of the disease. Using the largest cohort to date, the European Prevention of Alzheimer's Dementia Longitudinal Cohort Study, we test the hypotheses that poor sleep is associated with core Alzheimer's disease CSF biomarkers cross-sectionally and predicts future increments of Alzheimer's disease pathology in people without identifiable symptoms of Alzheimer's disease at baseline. This study included 1168 adults aged over 50 years with CSF core Alzheimer's disease biomarkers (total tau, phosphorylated tau and amyloid-beta), cognitive performance, and sleep quality (Pittsburgh sleep quality index questionnaire) data. We used multivariate linear regressions to analyse associations between core Alzheimer's disease biomarkers and the following Pittsburgh sleep quality index measures: total score of sleep quality, binarized score (poor sleep categorized as Pittsburgh sleep quality index > 5), sleep latency, duration, efficiency and disturbance. On a subsample of 332 participants with CSF taken at baseline and after an average period of 1.5 years, we assessed the effect of baseline sleep quality on change in Alzheimer's disease biomarkers over time. Cross-sectional analyses revealed that poor sleep quality (Pittsburgh sleep quality index total > 5) was significantly associated with higher CSF t-tau; shorter sleep duration (9 versus 0) was associated with lower CSF amyloid-beta. Longitudinal analyses showed that greater sleep disturbances (1-9 versus 0 and >9 versus 0) were associated with a decrease in CSF Aβ42 over time. This study demonstrates that self-reported poor sleep quality is associated with greater Alzheimer's disease-related pathology in cognitively unimpaired individuals, with longitudinal results further strengthening the hypothesis that disrupted sleep may represent a risk factor for Alzheimer's disease. This highlights the need for future work to test the efficacy of preventive practices, designed to improve sleep at pre-symptomatic stages of disease, on reducing Alzheimer's disease pathology