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Dillon, W.

Publications and source records attributed to Dillon, W..

2 recordsLinked to original sources

Mechanistic pathways of tick exposure risk in native and invaded plant communities

Plant invasions may alter disease vector abundance by several mechanistic pathways, including modifying microclimates that influence vector survival or changing habitats to influence host use. Here, we used a field experiment and observational data to evaluate multiple mechanistic pathways (tick survival and host abundance) by which plant invasions may alter vector-borne disease risk using the common disease vector lone star tick (Amblyomma americanum), its preeminent host white-tailed deer (Odocoileus virginianus), and the widespread invasive cogongrass (Imperata cylindrica) in the southeastern USA. In the field experiment, ticks survived over 50% longer in areas dominated by the invasive plant compared to those with only native plant species. Invaded areas had lower temperatures and higher relative humidity, yielding a lower vapor pressure deficit (VPD) that likely reduced tick desiccation. The observational study showed similar average tick abundance in native and invaded plant communities and no difference in wildlife host (white-tailed deer) activity between plant communities. However, there was a positive relationship between tick abundance and white-tailed deer activity, but only in native areas. Together, these results suggest that more favorable microclimate conditions resulting in greater tick longevity are the dominant driver of tick abundance in invaded areas, while tick abundance in native-dominated areas may be promoted, at least in part, by white-tailed deer activity. Our results demonstrate that plant invasions can affect multiple, potentially counteracting mechanistic pathways that contribute to tick exposure risk. The complexity of these relationships highlights the need for better understanding of how invasive species and other global change drivers influence disease vectors and, ultimately, disease transmission.

ecology↗

Lipid associated polygenic enrichment in Alzheimer’s disease

Cardiovascular (CV) and lifestyle associated risk factors (RFs) are increasingly recognized as important for Alzheimers disease (AD) pathogenesis. Beyond the [isin]4 allele of apolipoprotein E (APOE), comparatively little is known about whether CV associated genes also increase risk for AD (genetic pleiotropy). Using large genome-wide association studies (GWASs) (total n > 500,000 cases and controls) and validated tools to quantify genetic pleiotropy, we systematically identified single nucleotide polymorphisms (SNPs) jointly associated with AD and one or more CV RFs, namely body mass index (BMI), type 2 diabetes (T2D), coronary artery disease (CAD), waist hip ratio (WHR), total cholesterol (TC), low-density (LDL) and high-density lipoprotein (HDL). In fold enrichment plots, we observed robust genetic enrichment in AD as a function of plasma lipids (TC, LDL, and HDL); we found minimal AD genetic enrichment conditional on BMI, T2D, CAD, and WHR. Beyond APOE, at conjunction FDR < 0.05 we identified 57 SNPs on 19 different chromosomes that were jointly associated with AD and CV outcomes including APOA4, ABCA1, ABCG5, LIPG, and MTCH2/SPI1. We found that common genetic variants influencing AD are associated with multiple CV RFs, at times with a different directionality of effect. Expression of these AD/CV pleiotropic genes was enriched for lipid metabolism processes, over-represented within astrocytes and vascular structures, highly co-expressed, and differentially altered within AD brains. Beyond APOE, we show that the polygenic component of AD is enriched for lipid associated RFs. Rather than a single causal link between genetic loci, RF and the outcome, we found that common genetic variants influencing AD are associated with multiple CV RFs. Our collective findings suggest that a network of genes involved in lipid biology also influence Alzheimers risk.

genetics↗