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We present data from a nationally representative 2017 survey of American adults. For heterosexual couples in the United States, meeting online has become the most popular way couples meet, eclipsing meeting through friends for the first time around 2013. Moreover, among the couples who meet online, the proportion who have met through the mediation of third persons has declined over time. We find that Internet meeting is displacing the roles that family and friends once played in bringing couples together.

Abstract As the Internet’s role in creating new couples continues to expand, now accounting for over a third of recently-formed U.S. couples, its impact on endogamy is increasingly consequential. While there are good reasons to expect greater diversity from online romantic sources, there are also good sociological reasons to predict greater assortativity online. Increases in the rates of interracial and interreligious couples within the U.S. have occurred seemingly in tandem with the rise of online dating, but the evidence connecting online romances and couple heterogeneity have been limited and mixed. Using a unique nationally-representative dataset collected in 2009 and 2017 on how U.S. couples met, and controlling for the diversity of their local geographies, I find that couples who met online are more likely to be interracial, interreligious, and of different college degree status, but also more similar in age. Couples who met online are not more nor less likely to cross political boundaries, however, and not more nor less likely to have educationally different mothers. These exogamy differences can vary by where on the Internet couples met. Population-level estimates suggest that only a small part of the recent changes in couple diversity can be directly attributed to couples meeting online, but there is the potential for more Internet-induced change if it continues to expand as the modal source of romance.

Adolescent societies—whether arising from weak, short-term classroom friendships or from close, long-term friendships—exhibit various levels of network clustering, segregation, and hierarchy. Some are rank-ordered caste systems and others are flat, cliquish worlds. Explaining the source of such structural variation remains a challenge, however, because global network features are generally treated as the agglomeration of micro-level tie-formation mechanisms, namely balance, homophily, and dominance. How do the same micro-mechanisms generate significant variation in global network structures? To answer this question we propose and test a network ecological theory that specifies the ways features of organizational environments moderate the expression of tie-formation processes, thereby generating variability in global network structures across settings. We develop this argument using longitudinal friendship data on schools (Add Health study) and classrooms (Classroom Engagement study), and by extending exponential random graph models to the study of multiple societies over time.

How people meet new friends changes throughout life in ways that change the potential for diverse friendships. This study presents results from the first U.S. survey with data on how respondents met their friends, specifically the two nonfamily friends they most often socialize with. The most common sources of new friendships shift across life from the dominance of schooling during youth, to the centrality of work in midlife, to neighbors and voluntary groups in later life. Educational homophily peaks for friendships made in midlife, and is strongest for friendships made in higher education and at work. Racial homophily generally declines as people age but is lowest for men in midlife, while decreasing later for women. Friendship sources largely account for life course changes in racial homophily, but not educational homophily. The racial homophily induced by friendship sources also changes as people age, but in different ways for women and men.

This article explores how the efficiency of Internet search is changing the way Americans find romantic partners. We use a new data source, the How Couples Meet and Stay Together survey. Results show that for 60 years, family and grade school have been steadily declining in their influence over the dating market. In the past 15 years, the rise of the Internet has partly displaced not only family and school, but also neighborhood, friends, and the workplace as venues for meeting partners. The Internet increasingly allows Americans to meet and form relationships with perfect strangers, that is, people with whom they had no previous social tie. Individuals who face a thin market for potential partners, such as gays, lesbians, and middle-aged heterosexuals, are especially likely to meet partners online. One result of the increasing importance of the Internet in meeting partners is that adults with Internet access at home are substantially more likely to have partners, even after controlling for other factors. Partnership rate has increased during the Internet era (consistent with Internet efficiency of search) for same-sex couples, but the heterosexual partnership rate has been flat.

Life-threatening thrombotic events and neurological symptoms are prevalent in COVID-19 and are persistent in patients with long COVID experiencing post-acute sequelae of SARS-CoV-2 infection 1 – 4 . Despite the clinical evidence 1 , 5 – 7 , the underlying mechanisms of coagulopathy in COVID-19 and its consequences in inflammation and neuropathology remain poorly understood and treatment options are insufficient. Fibrinogen, the central structural component of blood clots, is abundantly deposited in the lungs and brains of patients with COVID-19, correlates with disease severity and is a predictive biomarker for post-COVID-19 cognitive deficits 1 , 5 , 8 – 10 . Here we show that fibrin binds to the SARS-CoV-2 spike protein, forming proinflammatory blood clots that drive systemic thromboinflammation and neuropathology in COVID-19. Fibrin, acting through its inflammatory domain, is required for oxidative stress and macrophage activation in the lungs, whereas it suppresses natural killer cells, after SARS-CoV-2 infection. Fibrin promotes neuroinflammation and neuronal loss after infection, as well as innate immune activation in the brain and lungs independently of active infection. A monoclonal antibody targeting the inflammatory fibrin domain provides protection from microglial activation and neuronal injury, as well as from thromboinflammation in the lung after infection. Thus, fibrin drives inflammation and neuropathology in SARS-CoV-2 infection, and fibrin-targeting immunotherapy may represent a therapeutic intervention for patients with acute COVID-19 and long COVID. Fibrin drives inflammation and neuropathology in SARS-CoV-2 infection, and fibrin-targeting immunotherapy may represent a therapeutic intervention for patients with long COVID.

Background Hyperexcitability of neuronal networks can lead to excessive release of the excitatory neurotransmitter glutamate, which in turn can cause neuronal damage by overactivating NMDA-type glutamate receptors and related signaling pathways. This process (excitotoxicity) has been implicated in the pathogenesis of many neurological conditions, ranging from childhood epilepsies to stroke and neurodegenerative disorders such as Alzheimer’s disease (AD). Reducing neuronal levels of the microtubule-associated protein tau counteracts network hyperexcitability of diverse causes, but whether this strategy can also diminish downstream excitotoxicity is less clear. Methods We established a cell-based assay to quantify excitotoxicity in primary cultures of mouse hippocampal neurons and investigated the role of tau in exicitotoxicity by modulating neuronal tau expression through genetic ablation or transduction with lentiviral vectors expressing anti-tau shRNA or constructs encoding wildtype versus mutant mouse tau. Results We demonstrate that shRNA-mediated knockdown of tau reduces glutamate-induced, NMDA receptor-dependent Ca 2+ influx and neurotoxicity in neurons from wildtype mice. Conversely, expression of wildtype mouse tau enhances Ca 2+ influx and excitotoxicity in tau-deficient ( Mapt −/− ) neurons. Reconstituting tau expression in Mapt −/− neurons with mutant forms of tau reveals that the tau-related enhancement of Ca 2+ influx and excitotoxicity depend on the phosphorylation of tau at tyrosine 18 (pY18), which is mediated by the tyrosine kinase Fyn. These effects are most evident at pathologically elevated concentrations of glutamate, do not involve GluN2B–containing NMDA receptors, and do not require binding of Fyn to tau’s major interacting PxxP motif or of tau to microtubules. Conclusions Although tau has been implicated in diverse neurological diseases, its most pathogenic forms remain to be defined. Our study suggests that reducing the formation or level of pY18-tau can counteract excitotoxicity by diminishing NMDA receptor-dependent Ca 2+ influx.

A core component of every blood program is the supply of safe blood and blood products. The elevated risk of transmission through these products is due to parvovirus B19 (B19V) resistance to the virus inactivation procedures. Our study aimed to screen asymptomatic blood donors for B19V at a tertiary care hospital in Chennai, Tamil Nadu, between September 2020 and June 2021. Sera from 106 healthy blood donors who tested negative for Human immunodeficiency virus (HIV), Hepatitis B surface antigen (HBsAg), Hepatitis C virus (HCV), syphilis, and malaria were tested for anti-B19V IgM and IgG using a qualitative indirect enzyme-linked immunosorbent assay (ELISA). In the study population, 23.5% (n = 25) of donors tested IgM positive, 38.6% (n = 41) tested IgG positive, and 7.5% (n = 8) tested positive for both IgM and IgG. A proportion of 61.3% (n = 65) of the blood donors tested IgG negative, suggesting they had no past B19V infection. B19V DNA was not detected in any of the subjects. The high seroprevalence of IgM indicates that blood donors may have been recently exposed to B19V, potentially posing a risk to immunocompromised individuals and those with hematological stress. Further longitudinal studies with a larger sample size are recommended to better understand the risk of B19V transfusion transmission.

Oxidative stress is a central part of innate immune-induced neurodegeneration. However, the transcriptomic landscape of central nervous system (CNS) innate immune cells contributing to oxidative stress is unknown, and therapies to target their neurotoxic functions are not widely available. Here, we provide the oxidative stress innate immune cell atlas in neuroinflammatory disease and report the discovery of new druggable pathways. Transcriptional profiling of oxidative stress–producing CNS innate immune cells identified a core oxidative stress gene signature coupled to coagulation and glutathione-pathway genes shared between a microglia cluster and infiltrating macrophages. Tox-seq followed by a microglia high-throughput screen and oxidative stress gene network analysis identified the glutathione-regulating compound acivicin, with potent therapeutic effects that decrease oxidative stress and axonal damage in chronic and relapsing multiple sclerosis models. Thus, oxidative stress transcriptomics identified neurotoxic CNS innate immune populations and may enable discovery of selective neuroprotective strategies. Oxidative stress can promote neurodegeneration. Akassoglou and colleagues describe Tox-seq, a functional single-cell RNA sequencing method to identify oxidative stress transcriptional signatures in CNS-resident cells. Tox-seq identified coagulation and glutathione-redox pathway genes that are coupled to oxidative stress and that could be targeted by the glutathione-regulating small molecule acivicin.

Microglial surveillance is a key feature of brain physiology and disease. Here, we found that G i -dependent microglial dynamics prevent neuronal network hyperexcitability. By generating Mg PTX mice to genetically inhibit G i in microglia, we show that sustained reduction of microglia brain surveillance and directed process motility induced spontaneous seizures and increased hypersynchrony after physiologically evoked neuronal activity in awake adult mice. Thus, G i -dependent microglia dynamics may prevent hyperexcitability in neurological diseases. Merlini, Rafalski et al. show that dynamic microglial brain surveillance prevents hyperexcitability and seizures by G i -dependent microglia–neuron interactions in response to evoked neuronal activity to maintain physiological network synchronization.