Project description:An Infinium microarray platform (GPL28271, HorvathMammalMethylChip40) was used to generate DNA methylation data from several tissues (skin, blood) in toothed whales and dolphins. Tissues: skin and blood.
Project description:An Infinium microarray platform (GPL28271, HorvathMammalMethylChip40) was used to generate DNA methylation data from skin samples of beluga whales, Maui's dolphin, and humpback whale. Tissue: Skin
Project description:An Infinium microarray platform (GPL28271, Horvath MammalMethylChip40) was used to generate DNA methylation data from skin samples of Hector's and Māui dolphins.
Project description:Climate warming is one factor increasing the severity of harmful algal blooms (HABs). Innovative exposure models are needed to understand how HABs affect brain health. Here, we examined HAB exposure on the brain transcriptome of dolphins found stranded in Florida’s Indian River Lagoon. We report the neurotoxin 2,4-diaminobutyric acid (2,4-DAB) is 2,900 times more concentrated in dolphin brains during bloom seasons compared to non-bloom seasons. The same dolphins show 536 differentially expressed genes whose enrichment reveal impairment in GABAergic synapses, basement membrane alteration, and Alzheimer’s disease (AD) risk factors that increase with each subsequent season. Dolphins also display concurrent AD-like neuropathological changes and elevated AD gene expression with 2,4-DAB exposure. Our study demonstrates disproportionate seasonal exposure to 2,4-DAB increases AD signatures in the brain transcriptome. As our climate warms, HABs will continue to intensify. Understanding the impact of HAB exposures will help to identify populations at risk for neurological illnesses.
Project description:Feeding a modified fish diet has been suggested to improve insulin sensitivity in bottlenose dolphins; however insulin sensitivity was not directly measured. Since demonstrating an improvement in insulin sensitivity is technically difficult in dolphins, we postulated that directional changes in the hormone axis: fibroblast growth factor 21 (FGF21)/Adiponectin/Ceramide (Cer), could provide further support to this hypothesis. Proteomic analysis of the serum proteins revealed few changes in serum proteins over the study period. In conclusion, changing the types of fish fed to dolphins resulted in increases in the insulin sensitizing hormone adiponectin and serum sphingosines consistent with an insulin sensitizing phenotype.
Project description:Epigenetic aging clocks based on DNA methylation patterns across the genome have emerged as a potential biomarker for risk of age-related diseases, like Alzheimer's disease (AD), and environmental and social stressors. However, methylation clocks have not been comprehensively validated in genetically diverse individuals. Here we evaluate a set of first-, second-, and third-generation methylation clocks in 621 AD patients and matched controls from African American, Hispanic, and White cohorts. The clocks are less accurate at predicting age in genetically admixed cohorts compared to the White cohort, especially for those with substantial African ancestry. This decreased accuracy holds in >2,500 individuals of European and African ancestry from three additional datasets. The clocks also fail to consistently identify age acceleration in admixed AD cases compared to controls. To explore potential causes for the lack of generalization of the clocks, we intersected clock CpGs with methylation, germline genetic variants, and methylation QTL (meQTL) data from global populations. We find differential methylation between African and European ancestry individuals is common for clock CpGs. Genetic variants rarely disrupt clock CpGs between populations, but a substantial fraction of clock CpGs have meQTL with significantly higher frequencies in African genetic ancestries. Our results demonstrate that methylation clocks often fail to predict age and AD risk when applied across populations and suggest avenues for improving their portability by considering differences in genetic and epigenetic patterns across human populations.