Biological Mechanisms of Antisocial Behavior and Moral Responsibility

We have long been concerned with understanding human behavior. Specifically, there has been an increased interest in biological explanations of antisocial behavior. These preliminary explanations, which stem from associations found in neuroscience, brain imaging and genetics, raise important ethical questions about free will, moral responsibility and blame. It is difficult to say at this point if these explanations lead individuals to believe that antisocial behavior is determined (at least to some degree), and should mitigate attributions of responsibility and blame, or if they make claims about who the individual is and should aggravate attributions of responsibility and blame. There are several reasons to completely disregard biological explanations of antisocial behavior in judgments about responsibility and blame. These include methodological issues with the science, misinterpretation of the scientific results, issues of human rights, disability, stigmatization, and exacerbation of racial and ethnic inequalities. As science continues to improve, several of the reasons to disregard these explanations will become obsolete and bring this dilemma back to the forefront. Notably, individuals already form beliefs about free will and use them to ascribe moral responsibility and blame. Evidence suggests that these views are malleable, and may be influenced by the motivation to punish, to discourage violations of norms, beliefs about individual affect, political views, and the desire to avoid discomfort. Science provides a better foundation for claims of moral responsibility and blame, as good science is reproducible and objective. This may be helpful in combatting current issues of racial and socioeconomic injustice that directly affect attributions of moral responsibility and blame. Lastly, biological explanations of antisocial behavior may be crucial in creating a shift from punitive models of criminal justice to a focus on rehabilitation. Ultimately, biological explanations of antisocial behavior may be able to differentiate which behavior is a product of disease or dysfunction, and which is not. Such a distinction, in combination with relevant application of moral values and principles, can help make more appropriate claims about mitigating or aggravating moral responsibility and blameworthiness for antisocial behavior

Toxoplasma gondii IgG Serointensity Is Positively Associated With Frailty

Background: Persistent inflammation related to aging (inflammaging) is exacerbated by chronic infections and contributes to frailty in older adults. We hypothesized associations between Toxoplasma gondii (T. gondii), a common parasite causing an oligosymptomatic unremitting infection, and frailty, and secondarily between T. gondii and previously reported markers of immune activation in frailty.Methods: We analyzed available demographic, social, and clinical data in Spanish and Portuguese older adults [N = 601; age: mean (SD) 77.3 (8.0); 61% women]. Plasma T. gondii immunoglobulin G (IgG) serointensity was measured with an enzyme-linked immunosorbent assay. The Fried criteria were used to define frailty status. Validated translations of Mini-Mental State Examination, Geriatric Depression Scale, and the Charlson Comorbidity Index were used to evaluate confounders. Previously analyzed biomarkers that were significantly associated with frailty in both prior reports and the current study, and also related to T. gondii serointensity, were further accounted for in multivariable logistic models with frailty as outcome.Results: In T. gondii-seropositives, there was a significant positive association between T. gondii IgG serointensity and frailty, accounting for age (p = .0002), and resisting adjustment for multiple successive confounders. Among biomarkers linked with frailty, kynurenine/tryptophan and soluble tumor necrosis factor receptor II were positively associated with T. gondii serointensity in seropositives (p < .05). Associations with other biomarkers were not significant.Conclusions: This first reported association between T. gondii and frailty is limited by a cross-sectional design and warrants replication. While certain biomarkers of inflammaging were associated with both T. gondii IgG serointensity and frailty, they did not fully mediate the T. gondii-frailty association.This work was supported in part by the Spanish Ministry of Science and Innovation: MCIN/AEI/10.13039/501100011033(grant PID2020-113788RB-I00); Xunta de Galicia (grant ED431B 2022/16); Ministry of Education, Culture and Sport (grant BEAGAL18/00142 to V.V.); and Ministry of Economy and Competitiveness, cofinanced by the European Social Fund (grant RYC-2015-18394 to L.L.-L.). Additionally supported, in part, by the University of Maryland School of Medicine Center for Research on Aging in Baltimore, Maryland; a Clinical Science Research & Development Service Merit Award, Office of Research and Development, U.S. Department of Veterans Affairs, Washington, District of Columbia (grant 1 I01 CX001310-01 to T.T.P.); a R01 grant from the National Institute on Aging, National Institutes of Health, Bethesda, Maryland (grant NIA R01 AG018859 to E.J.K.); and by the Military and Veteran Microbiome: Consortium for Research and Education in Aurora, Colorado (L.A.B., A.J.H., C.A.L., T.T.P.). The opinions expressed in the article belong to the authors and cannot be construed as official positions or opinions of the funders, including the U.S. Veterans Affairs Administration and the National Institutes of Health. Data collected and used for the analyses reported in this article are not available because the initial consent did not include this sharing and because other primary analyses have not been completed. Funding for open access charge: Universidade da Coruna/CISUG

Biological and Psychological Factors Determining Neuropsychiatric Outcomes in COVID-19

Purpose of Review: We present biological and psychological factors implicated in psychiatric manifestations of SARS-CoV-2, as well as its neuroinvasive capability and immune pathophysiology.Recent Findings: Preexisting mental illness leads to worse clinical outcomes in COVID-19. The presence of the virus was reported in the cerebrospinal fluid (CSF) and brain tissue post-mortem. Most common psychiatric manifestations include delirium, mood disorders, anxiety disorders, and posttraumatic stress disorder. “Long-COVID” non-syndromal presentations include “brain-fogginess,” autonomic instability, fatigue, and insomnia.Summary: SARS-CoV-2 infection can trigger prior vulnerabilities based on the priming of microglia and other cells, induced or perpetuated by aging and mental and physical illnesses. COVID-19 could further induce priming of neuroimmunological substrates leading to exacerbated immune response and autoimmunity targeting structures in the central nervous system (CNS), in response to minor immune activating environmental exposures, including stress, minor infections, allergens, pollutants, and traumatic brain injury