Åtgärder för att gynna biologisk mångfald i slättbygder - En kunskapssammanställning

Trots att jordbrukslandskapet enbart utgör en liten andel av Sveriges totala yta så är många av de arter som minskat i antal och utbredning knutna till just detta. Om inte förlusten av biologisk mångfald i jordbrukslandskapet bryts kan detta leda till att Sverige inte lever upp till konventionen om biologisk mångfald och till att viktiga ekosystemtjänster i jordbrukslandskapet som pollination och skadedjursbekämpning hotas. En viktig orsak till den minskade biologiska mångfalden är jordbrukets intensifiering, d.v.s. olika metoder som används för att öka skörden. Ökad användning av konstgödning och växtskyddsmedel har medfört att organismer har svårare att klara sig ute på fälten samtidigt som den ekologiska variationsrikedomen i landskapet minskat genom att naturbetesmarker, kantzoner och andra småbiotoper försvunnit. Längst har denna utveckling gått i slättbygden som också drabbats hårdast av förlust av biologisk mångfald. Miljöstöden har visat sig otillräckliga för att bevara den biologiska mångfalden i slättbygden. Det finns därför ett behov av enkla åtgärder som lantbrukare kan vidta för att bevara eller öka den biologiska mångfalden på gården. Det är viktigt att åtgärder som rekommenderas för att öka den biologiska mångfalden på gården är baserade på fakta. Vi har därför sökt efter och sammanställt publicerade vetenskapliga studier som utvärderat sådana åtgärder. De åtgärder som behandlas är av tre typer. För det första kan man ändra odlingssystemet så att brukandet av marken generellt sett blir mindre intensiv vilket leder till att den ekologiska variationsrikedomen på fältnivå ökar. I den här rapporten presenterar vi en sådan åtgärd, ekologisk odling. En speciell åtgärd är allmogeåkrar, där den extensiva odlingen genomförs i en betydligt mindre skala. För det andra, i landskap där inslaget av mer eller mindre naturliga habitat som naturbetesmarker, obrukade kantzoner och småbiotoper minskat kraftigt, kan åtgärder som ökar kvalitén på de återstående naturliga habitaten eller som skapar nya habitat vara sätt att öka den biologiska mångfalden. I den här rapporten tar vi upp ett antal olika alternativ så som skötsel av befintliga kantzoner, anläggande av vegetationsremsor längs fältkanter eller kring åkerholmar, och skapande av dammar. För det tredje kan åtgärder göras som direkt skyddar eller skapar boplatser eller bidrar med födoresurser för organismer som är hotade i dagens jordbrukslandskap. Vi finner att det finns starkt vetenskapligt stöd för att många, men inte alla, åtgärder påverkar åtminstone vissa organismgrupper positivt. Flera av åtgärderna har tydligare effekt på biologisk mångfald i slättbygder, där de kan återställa en del av den förlorade mångfalden, än i mindre intensivt odlade bygder där mycket av mångfalden fortfarande finns kvar. Många av de vetenskapliga utvärderingarna av åtgärdernas effekter visar på ökad lokal täthet eller mångfald av organismer, men oftast saknas analyser av om organismer som är sällsynta på en regional nivå gynnas. När man försöker gynna mångfalden med lokala åtgärder, som anlagda habitat, saknas i vissa fall undersökningar som visar att organismerna inte bara attraheras till åtgärden, utan att populationerna också påverkas positivt

4. Farmland Conservation

Expert assessors Lynn V. Dicks, University of Cambridge, UK Ian Hodge, University of Cambridge, UK Clunie Keenleyside, Institute for European Environmental Policy, UK Will Peach, Royal Society for the Protection of Birds, UK Nicola Randall, Harper Adams University, UK Jörn Scharlemann, United Nations Environment Programme — World Conservation Monitoring Centre, UK Gavin Siriwardena, British Trust for Ornithology, UK Henrik Smith, Lund University, Sweden Rebecca K. Smith, University of Cambrid..

Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects

Copy number variants (CNVs) have been strongly implicated in the genetic etiology of schizophrenia (SCZ). However, genome-wide investigation of the contribution of CNV to risk has been hampered by limited sample sizes. We sought to address this obstacle by applying a centralized analysis pipeline to a SCZ cohort of 21,094 cases and 20,227 controls. A global enrichment of CNV burden was observed in cases (OR=1.11, P=5.7×10−15), which persisted after excluding loci implicated in previous studies (OR=1.07, P=1.7 ×10−6). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 ×10−11) and neurobehavioral phenotypes in mouse (OR = 1.18, P= 7.3 ×10−5). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by non-allelic homologous recombination

What Works in Conservation 2018

This book provides an assessment of the effectiveness of 1277 conservation interventions based on summarized scientific evidence. The 2018 edition contains new chapters covering practical global conservation of primates, peatlands, shrublands and heathlands, management of captive animals as well as an extended chapter on control of freshwater invasive species. Other chapters cover global conservation of amphibians, bats, birds and forests, conservation of European farmland biodiversity and some aspects of enhancing natural pest control, enhancing soil fertility and control of freshwater invasive species. It contains key results from the summarized evidence for each conservation intervention and an assessment of the effectiveness of each by international expert panels. The accompanying website www.conservationevidence.com describes each of the studies individually, and provides full references

No Reliable Association between Runs of Homozygosity and Schizophrenia in a Well-Powered Replication Study

It is well known that inbreeding increases the risk of recessive monogenic diseases, but it is less certain whether it contributes to the etiology of complex diseases such as schizophrenia. One way to estimate the effects of inbreeding is to examine the association between disease diagnosis and genome-wide autozygosity estimated using runs of homozygosity (ROH) in genome-wide single nucleotide polymorphism arrays. Using data for schizophrenia from the Psychiatric Genomics Consortium (n = 21,868), Keller et al. (2012) estimated that the odds of developing schizophrenia increased by approximately 17% for every additional percent of the genome that is autozygous (β = 16.1, CI(β) = [6.93, 25.7], Z = 3.44, p = 0.0006). Here we describe replication results from 22 independent schizophrenia case-control datasets from the Psychiatric Genomics Consortium (n = 39,830). Using the same ROH calling thresholds and procedures as Keller et al. (2012), we were unable to replicate the significant association between ROH burden and schizophrenia in the independent PGC phase II data, although the effect was in the predicted direction, and the combined (original + replication) dataset yielded an attenuated but significant relationship between Froh and schizophrenia (β = 4.86,CI(β) = [0.90,8.83],Z = 2.40,p = 0.02). Since Keller et al. (2012), several studies reported inconsistent association of ROH burden with complex traits, particularly in case-control data. These conflicting results might suggest that the effects of autozygosity are confounded by various factors, such as socioeconomic status, education, urbanicity, and religiosity, which may be associated with both real inbreeding and the outcome measures of interest

Age at first birth in women is genetically associated with increased risk of schizophrenia

Prof. Paunio on PGC:n jäsenPrevious studies have shown an increased risk for mental health problems in children born to both younger and older parents compared to children of average-aged parents. We previously used a novel design to reveal a latent mechanism of genetic association between schizophrenia and age at first birth in women (AFB). Here, we use independent data from the UK Biobank (N = 38,892) to replicate the finding of an association between predicted genetic risk of schizophrenia and AFB in women, and to estimate the genetic correlation between schizophrenia and AFB in women stratified into younger and older groups. We find evidence for an association between predicted genetic risk of schizophrenia and AFB in women (P-value = 1.12E-05), and we show genetic heterogeneity between younger and older AFB groups (P-value = 3.45E-03). The genetic correlation between schizophrenia and AFB in the younger AFB group is -0.16 (SE = 0.04) while that between schizophrenia and AFB in the older AFB group is 0.14 (SE = 0.08). Our results suggest that early, and perhaps also late, age at first birth in women is associated with increased genetic risk for schizophrenia in the UK Biobank sample. These findings contribute new insights into factors contributing to the complex bio-social risk architecture underpinning the association between parental age and offspring mental health.Peer reviewe

Genetic correlation between amyotrophic lateral sclerosis and schizophrenia

A. Palotie on työryhmän Schizophrenia Working Grp Psychiat jäsen.We have previously shown higher-than-expected rates of schizophrenia in relatives of patients with amyotrophic lateral sclerosis (ALS), suggesting an aetiological relationship between the diseases. Here, we investigate the genetic relationship between ALS and schizophrenia using genome-wide association study data from over 100,000 unique individuals. Using linkage disequilibrium score regression, we estimate the genetic correlation between ALS and schizophrenia to be 14.3% (7.05-21.6; P = 1 x 10(-4)) with schizophrenia polygenic risk scores explaining up to 0.12% of the variance in ALS (P = 8.4 x 10(-7)). A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (odds ratio 1.08-1.26) but this would require very large studies to observe epidemiologically. We identify five potential novel ALS-associated loci using conditional false discovery rate analysis. It is likely that shared neurobiological mechanisms between these two disorders will engender novel hypotheses in future preclinical and clinical studies.Peer reviewe

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe