Zionsville Community High School (ZCHS) is a 4-year public high school located in Boone County, Zionsville, Indiana, United States. It is the only high school in the Zionsville Community School Corporation.
Populations face complex selective landscapes shaped by a combination of ecological pressures, and increasingly, novel anthropogenic challenges. Such selective forces may limit evolutionary responses and push populations to the brink of extinction, particularly when natural and anthropogenic selection target traits constrained by functional demands or pleiotropy. How ecological and human-induced pressures interact to shape molecular evolution remains poorly understood. In the western United States, the caddisfly Limnephilus flavastellus has been simultaneously exposed to a natural toxin, tetrodotoxin (TTX), by feeding on Rough-Skinned Newt ( Taricha granulosa ) eggs, as well as anthropogenic insecticides such as DDT and pyrethroids applied widely in the environment. These toxins have distinct effects on insect voltage-gated sodium channels (Na v 1), with TTX blocking sodium influx while pyrethroids prolonging channel activation. Using whole-animal assays to determine lethal concentrations (LC 50 ), we demonstrate that L. flavastellus exhibits 4.8-fold greater TTX resistance and 3.7-fold greater pyrethroid resistance compared to a closely related caddisfly species that does not experience these toxins in the wild. We used transcriptomic sequencing and comparative genomics to determine the genetic basis of these phenotypes, discovering 77 unique amino acid substitutions in Na v 1, including 4 in pore-forming regions associated with TTX resistance and 5 in regions linked to pyrethroid resistance in L. flavastellus . These mutations correspond to known resistance-conferring substitutions in other TTX-resistant species and insecticide-resistant species, demonstrating convergent evolution in the caddisfly sodium channel. These large-effect mutations coupled with many potentially compensatory mutations have important implications for our understanding of protein evolution and suggest that despite a complex selective landscape operating on a protein critical to cell electrophysiology, functional constraints on adaptive evolution can still be overcome.
Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons and the aggregation of α-synuclein, with increasing evidence implicating environmental factors and neuroimmune dysfunction in its pathogenesis. Micro- and nanoplastics (MNPs), ubiquitous environmental pollutants generated from plastic degradation, have recently emerged as potential biological stressors capable of entering the human body and accumulating in sensitive tissues, including the brain. Due to their small size, environmental persistence, and capacity to carry toxic additives and environmental contaminants, these particles can induce oxidative stress, impair mitochondrial and lysosomal function, and activate both innate and adaptive immune responses. This review summarizes current evidence linking microplastic exposure to neuroinflammatory processes relevant to PD, with a particular focus on microglial activation, astrocyte reactivity, peripheral immune involvement, and dysfunction of the gut–brain axis. Although a direct causal relationship between MNPs and PD has yet to be established, and direct human epidemiological evidence linking MNP exposure to PD is currently absent, the immunotoxic and neuroinflammatory effects of these particles suggest that they may contribute to disease susceptibility and progression. Elucidating the interactions between MNPs and neuroimmune pathways may help refine current frameworks linking environmental exposure, neuroimmune dysfunction, and PD susceptibility.
