Elliot C. Nelson

This paper conducts a multi-ancestry GWAS of stimulant use disorder, identifies 19 genome-wide significant loci, and finds genetic correlations with other psychiatric and substance use disorders.

This study shows that Cnih3 deletion in mice impairs spatial memory, reward-cue association, and fentanyl self-administration, with potential sex-specific effects on opioid use.

This study performs a multi-ancestral GWAS of DSM-defined nicotine dependence, finding genetic correlations with other substance use disorders and health traits, and identifying a strong general addiction liability factor.

This study identifies genetic correlations between substance use and aging indices, finding causal effects of tobacco and alcohol use on aging with alcohol effects dependent on quantity.

The paper profiles hippocampal transcriptomes across estrous cycles in mice, identifies estrous-responsive genes, and shows Cnih3 deletion disrupts estrous-specific gene expression patterns.

The paper examines genetic overlaps between suicide-related behaviors and substance use disorders using GWAS summary statistics and finds significant genetic correlations but little evidence of causation.

This study investigates the role of CNIH3 in spatial memory, finding sex-specific effects where CNIH3 deficiency impairs spatial memory in female mice but not males.

This study uses scRNA-seq to show chronic opioid use suppresses antiviral gene programs in immune cells, both acutely and chronically, highlighting potential immune system harm.

The paper compares genome-wide data from opioid use and dependence cases to identify genetic associations and differences between exposure and dependence.

This paper identifies novel pleiotropic risk loci for melanoma and nevus density, implicating multiple biological pathways and gene expression under MITF regulation.