A mutual information algorithm points to macrophage activation syndrome as a specific pathogenic mechanism in COVID-19, correlated with disease severity, which could be used to monitor disease and therapeutics.
Cross-species transcriptomic analysis and high-throughput behavioral assays in a Drosophila model of Huntington's disease show that downregulation of glial genes involved in synaptic function compensates for disease-related excitotoxicity.
A cell-surface receptor called Gpr52 is able to lower the levels of the disease-causing protein mutant huntingtin and suppress its toxicity when knocked-down, making this receptor a promising drug target in Huntington's disease.
In mouse models of Huntington's disease, striatal spiny projection neurons up-regulate dendritic potassium channels, which impairs their normal function, but a zinc finger gene therapy can reverse this deficit.
Human cullin-RING ligases are buffered to a much greater extent than had been previously appreciated, and the roles of ubiquitin chain extension enzymes are far more nuanced at physiological concentrations.