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Over the last decades, the social context has been characterized by uncertainty, complexity, and inequalities, with significant impacts on people, groups, and communities. Covid-19 Pandemic has accentuated social discriminations, as inequalities affecting women (World Health Organization, 2018), with repercussions on general income, health, education (Office for National Statistics, 2021) that have been exhausting people, the economic system, and the welfare state (Antonicelli et al., 2020). To cope with these difficulties, on april 10, 2020 the Italian Prime Minister appointed a Task Force of 17 experts with scientific and applicative skills in social and economic fields. Within a short time, the Task Force aimed at identifying practical solutions priming the relaunch of the country. Given the women's central role in the country's social and economic development, in the final version of the Task Force plan, Gender Equality was indicated as the third—strategic and innovative—axis, together with Digitization and Green Economy. Its rationale was to promote gender equality in every action, with an allocation of dedicated economic resources. Specifically, the Task Force's Working Group named "Individuals, Families, and Society" proposed specific initiatives aimed at recognizing and bridging the gender gaps in the various areas, and measures to support vulnerable people. This contribution will focus on the central role that the Task Force has played in encouraging systematic attention to women, considering their needs and the social-economic impacts on their choices and well-being. It will illustrate the Task Force's internal dynamics (there were four women out of 17 people, then increased), the process of inclusion of different perspectives, both gender and multidisciplinary, and the practices suggested for the post-pandemic rebuilding. The final goal will be to show the inability to promote innovation, resilience and sustainability, without working with and for the community. As shown by the Italian Task Force, an innovative change must consider a multiplicity of perspectives that reflects the complexity of reality, even in the political and decision-making debate. Therefore, it's central to build multidisciplinary teams that include various professionals from the social sectors, as Social Psychology, Sociology, Pedagogy, Political Philosophy, Demography, and Social Statistics, both women and men.

This is the final version. Available from Elsevier via the DOI in this record. ; Genome-wide association studies (GWASs) have been effective approaches to dissect common genetic variability underlying complex diseases in a systematic and unbiased way. Recently, GWASs have led to the discovery of over 20 susceptibility loci for Alzheimer's disease (AD). Despite the evidence showing the contribution of these loci to AD pathogenesis, their genetic architecture has not been extensively investigated, leaving the possibility that low frequency and rare coding variants may also occur and contribute to the risk of disease. We have used exome and genome sequencing data to analyze the single independent and joint effect of rare and low-frequency protein coding variants in 9 AD GWAS loci with the strongest effect sizes after APOE (BIN1, CLU, CR1, PICALM, MS4A6A, ABCA7, EPHA1, CD33, and CD2AP) in a cohort of 332 sporadic AD cases and 676 elderly controls of British and North-American ancestry. We identified coding variability in ABCA7 as contributing to AD risk. This locus harbors a low-frequency coding variant (p.G215S, rs72973581, minor allele frequency = 4.3%) conferring a modest but statistically significant protection against AD (p-value = 0.024, odds ratio = 0.57, 95% confidence interval = 0.41-0.80). Notably, our results are not driven by an enrichment of loss of function variants in ABCA7, recently reported as main pathogenic factor underlying AD risk at this locus. In summary, our study confirms the role of ABCA7 in AD and provides new insights that should address functional studies. ; This study was supported by the Alzheimer's Research UK, the Medical Research Council (MRC), the Wellcome Trust/MRC Joint Call in Neurodegeneration award (WT089698) to the UK Parkinson's Disease Consortium (whose members are from the University College London Institute of Neurology, the University of Sheffield, and the MRC Protein Phosphorylation Unit at the University of Dundee), grants (P50 AG016574, U01 AG006786, and R01 AG18023), the National Institute for Health Research Biomedical Research Unit in Dementia at University College London Hospitals, University College London; an anonymous donor, the Big Lottery (to Dr. Morgan); a fellowship from Alzheimer's Research UK (to Dr. Guerreiro); and the Intramural Research Programs of the National Institute on Aging and the National Institute of Neurological Disease and Stroke, National Institutes of Health (Department of Health and Human Services Project number, ZO1 AG000950-10). The MRC London Neurodegenerative Diseases Brain Bank and the Manchester Brain Bank from Brains for Dementia Research are jointly funded from ARUK and AS. This work was supported in part by the Intramural Research Program of the National Institute on Aging, National Institutes of Health, Department of Health and Human Services, project number ZO1 AG000950-10. Samples from the National Cell Repository for Alzheimer's Disease (NCRAD), which receives government support under a cooperative agreement grant (U24 AG21886) awarded by the National Institute on Aging (NIA), were used in this study. NIH grant R01 AG042611 to Kauwe J.