Climate trauma refers to the chronic mental health sequalae of climate disaster events. We have previously shown evidence for such trauma with accompanying anxiety and depression symptoms after Californias 2018 Camp Fire wildfire. Here, we investigate whether this climate trauma also impacts cognitive decision-making and its neural correlates. One year after the wildfire, we recruited three groups - those directly exposed (n = 27), indirectly exposed (community members who witnessed the wildfire but not directly exposed, n = 21), versus non-exposed controls (n = 27). Participants performed a decision-making task that led to immediate and cumulative point rewards on each trial with simultaneous electroencephalography (EEG) recordings. We evaluated Win-Stay behavior in choosing to stay with the greater expected value (cumulative reward) option. Directly-exposed individuals showed significantly reduced Win-Stay behavior relative to the other groups. EEG analyses showed significantly greater parietal alpha activity for the selected choice and ensuing rewards in directly fire-exposed individuals, with an underlying cortical source of this activity in posterior cingulate cortex. Overall, these findings suggest that climate trauma may significantly impact neuro-cognitive processing in the context of value-based decision-making, which may serve as a useful biomarker target for future mental health interventions in climate change impacted communities.

Vaccine adjuvants enhance and prolong pathogen-specific protective immune responses. Recent reports indicate that host factors-such as aging, pregnancy, and genetic polymorphisms-influence efficacies of vaccines adjuvanted with Toll-like receptor (TLR) or known pattern-recognition receptor (PRR) agonists. Although PRR independent adjuvants (e.g., oil-in-water emulsion and saponin) are emerging, these adjuvants induce some local and systemic reactogenicity. Hence, new TLR and PRR-independent adjuvants that provide greater potency alone or in combination without compromising safety are highly desired. Previous cell-based high-throughput screenings yielded a small molecule 81 [N-(4-chloro-2,5-dimethoxyphenyl)-4-ethoxybenzenesulfonamide], which enhanced lipopolysaccharide-induced NF-κB and type I interferon signaling in reporter assays. Here compound 81 activated innate immunity in primary human peripheral blood mononuclear cells and murine bone marrow-derived dendritic cells (BMDCs). The innate immune activation by 81 was independent of TLRs and other PRRs and was significantly reduced in mitochondrial antiviral-signaling protein (MAVS)-deficient BMDCs. Compound 81 activities were mediated by mitochondrial dysfunction as mitophagy inducers and a mitochondria specific antioxidant significantly inhibited cytokine induction by 81. Both compound 81 and a derivative obtained via structure-activity relationship studies, 2F52 [N-benzyl-N-(4-chloro-2,5-dimethoxyphenyl)-4-ethoxybenzenesulfonamide] modestly increased mitochondrial reactive oxygen species and induced the aggregation of MAVS. Neither 81 nor 2F52 injected as adjuvants caused local or systemic toxicity in mice at effective concentrations for vaccination. Furthermore, vaccination with inactivated influenza virus adjuvanted with 2F52 demonstrated protective effects in a murine lethal virus challenge study. As an unconventional and safe adjuvant that does not require known PRRs, compound 2F52 could be a useful addition to vaccines.