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

A passive and objective measure of recognition memory in Alzheimer’s disease using Fastball memory assessment

Earlier diagnosis of Alzheimer’s disease requires biomarkers sensitive to associated structural and functional changes. While considerable progress has been made in the development of structural biomarkers, functional biomarkers of early cognitive change, unconfounded by effort, practice and level of education, are still needed. We present Fastball, a new EEG method for the passive and objective measurement of recognition memory, that requires no behavioural memory response or comprehension of the task . Younger adults, older adults and Alzheimer’s disease patients (n = 20 per group) completed the Fastball task, lasting just under 3 min. Participants passively viewed rapidly presented images and EEG assessed their automatic ability to differentiate between images based on previous exposure, i.e. old/new. Participants were not instructed to attend to previously seen images and provided no behavioural response. Following the Fastball task, participants completed a two-alternative forced choice (2AFC) task to measure their explicit behavioural recognition of previously seen stimuli. Fastball EEG detected significantly impaired recognition memory in Alzheimer’s disease compared to healthy older adults (P < 0.001, Cohen’s d = 1.52), whereas behavioural recognition was not significantly different between Alzheimer’s disease and healthy older adults. Alzheimer’s disease patients could be discriminated with high accuracy from healthy older adult controls using the Fastball measure of recognition memory (AUC = 0.86, P < 0.001), whereas discrimination performance was poor using behavioural 2AFC accuracy (AUC = 0.63, P = 0.148). There were no significant effects of healthy ageing, with older and younger adult controls performing equivalently in both the Fastball task and behavioural 2AFC task. Early diagnosis of Alzheimer’s disease offers potential for early treatment when quality of life and independence can be retained through disease modification and cognitive enhancement. Fastball provides an alternative way of testing recognition responses that holds promise as a functional marker of disease pathology in stages where behavioural performance deficits are not yet evident. It is passive, non-invasive, quick to administer and uses cheap, scalable EEG technology. Fastball provides a new powerful method for the assessment of cognition in dementia and opens a new door in the development of early diagnosis tools

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

Standards of Practice in Acute Ischemic Stroke Intervention: International Recommendations

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Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease

We sought to identify new susceptibility loci for Alzheimer's disease through a staged association study (GERAD+) and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium (ADGC) in a companion paper. We undertook a combined analysis of four genome-wide association datasets (stage 1) and identified ten newly associated variants with P ≤ 1 × 10−5. We tested these variants for association in an independent sample (stage 2). Three SNPs at two loci replicated and showed evidence for association in a further sample (stage 3). Meta-analyses of all data provided compelling evidence that ABCA7 (rs3764650, meta P = 4.5 × 10−17; including ADGC data, meta P = 5.0 × 10−21) and the MS4A gene cluster (rs610932, meta P = 1.8 × 10−14; including ADGC data, meta P = 1.2 × 10−16) are new Alzheimer's disease susceptibility loci. We also found independent evidence for association for three loci reported by the ADGC, which, when combined, showed genome-wide significance: CD2AP (GERAD+, P = 8.0 × 10−4; including ADGC data, meta P = 8.6 × 10−9), CD33 (GERAD+, P = 2.2 × 10−4; including ADGC data, meta P = 1.6 × 10−9) and EPHA1 (GERAD+, P = 3.4 × 10−4; including ADGC data, meta P = 6.0 × 10−10)

Small areas of wildflower grassland in urban areas support significant species richness and abundance of pollinating insects

Diversity of invertebrate pollinators is essential in supporting flowering plant species richness, including agricultural crops. In the UK, losses are reported for bees, hoverflies, butterflies and moths. Urban green spaces are essential refugia for these groups, and restoration of these areas can improve pollinator diversity through improved floral resources.&lt;br/&gt; 2. Our research aimed to compare two differently managed areas of urban amenity grassland for their insect pollinators, with transect surveys of butterflies, bumblebees, solitary bees and hoverflies.&lt;br/&gt; 3. Our results revealed that even in an urban matrix, a small area of wildflower meadow had significantly higher insect abundance and species richness than a comparable amenity grassland. Both abundance and species richness of pollinating insects was positively related to floral species richness.&lt;br/&gt; 4. The wildflower grassland supported a number of notable solitary bee species and numerous hoverflies, although visitation by solitary bees was confined to only a small number of flowering plants, exhibiting visitation specialisation; however many of these plant species were not visited by other taxa

Effects of a combination of subchronic tobacco smoke exposure and lipopolysaccharide administration on pulmonary inflammation in the mouse

Chronic Obstructive Pulmonary Disease (COPD) is characterised by a predominantly irreversible restriction of airflow and often by acute exacerbations (AECOPD). These exacerbations are defined as a worsening of symptoms that result in a need to alter medication and are associated with an altered inflammatory response and a decline in lung function. Tobacco smoking is widely accepted as the main causative agent for COPD, with the majority of exacerbations being associated with subsequent bacterial or viral infection. Our aim was to develop a model that would mimic aspects of the altered inflammatory response observed in a bacteria-induced AECOPD. We combined multiple wholebody tobacco smoke (TS) exposures with the administration of the bacterial mimetic lipopolysaccharide (LPS). Each week for the first five weeks, female Balb/c mice (n=8-10 per group) were exposed twice a day to 30 minutes of either TS (750µg/l wet total particulate matter) or room air (RA) on days 1-5. On days 6 and 7 they were rested. During week six, the protocol was the same for the first two days. On the morning of day three LPS (0.3mg/kg; E.coli 0111:B4) or saline (0.9%w/v) were administered intranasally under isoflurane anaesthesia followed 5 hours later by TS or RA exposure. Twenty four hours after LPS administration animals were terminally anaesthetised (Fentanyl citrate 0.8mg/kg, Fluanisone 25mg/kg and Midazolam 12.45mg/kg i.p.) and the trachea cannulated. Bronchoalveolar lavage (BAL) was then performed to assess cell influx (Table1), cytokine levels and cytotoxicity. Data are expressed as the mean ±SEM with n=8-10 animals per group. BAL total cells were elevated in mice exposed to the combination of LPS and TS compared to those exposed to TS alone. However, the increase in total cells, compared to RA/saline controls, was lower in the mice exposed to LPS/TS compared to those exposed to LPS alone (Table 1). Neutrophils showed a comparable profile. Interleukin-6 (IL-6) concentrations in the BAL were significantly elevated in the RA/LPS (1687±176pg/ml) animals compared to RA/Saline (57±9 pg/ml) mice. They were also significantly elevated in the TS/LPS animals (745±125 pg/ml) but to a lesser extent. Interleukin-1β and keratinocyte cytokine (KC) showed similar profiles. Lactate dehydrogenase (LDH) activity, a marker of cytotoxicity, was highest in the BAL of TS/LPS treated animals (1.9±0.3 absorbance units (AU)) compared with either the RA/LPS animals (1.3±0.2AU), the TS/Saline mice (0.9±0.1) or the RA/Saline mice (0.2±0). These data indicate that certain aspects of the inflammatory response to LPS are reduced after 6 weeks TS exposure. This animal model may be useful for investigating the altered inflammatory response observed during an AECOPD. Table 1: Effect of LPS and tobacco smoke exposure on cell numbers in the BAL. Treatment groups RA/Saline RA/LPS TS/Saline TS/LPS Total cells 100 ± 14 1438 ±167(###) 477 ± 31 992 ± 166(###) Neutrophils 2 ± 1 1253 ± 155(###) 267 ± 19 736 ± 128(###) Macrophages 98 ± 14 183 ± 30 208 ± 23(#) 256 ± 47(##) Data expressed as mean cells x 103/ml ± sem. (Kruskal-Wallis followed by Dunn’s post test was used # p<0.05, ## p<0.01, ### p<0.001 compared to RA/Saline control