Terao et al. demonstrated how dysregulated cholesterol metabolism drives macrophage senescence and the development of subretinal drusenoid deposits in mice. LXR/CD38 signaling activated by cholesterol reduces NAD+ availability and promotes macrophage senescence. Senolytic agents targeting NAD+ decline and senescent macrophages are a potential therapeutic option against early AMD.
Related Posts
Distributed X chromosome inactivation in brain circuitry is associated with X-linked disease penetrance of behavior
Szelenyi et al. demonstrate that adult brain XCI is systematically biased toward maternal X-active cells, which is sufficient for disease penetrance of the X-linked Fmr1-KO allele. Furthermore, local XCI mosaicism distinguishes phenotypic outcomes of individuals based on mutant X-active cells populating […]
Neospora caninum, a Protozoan Killing Dogs, “Might Be Key” to “Total Regression of Tumors”
Neosporosis, caused by the intracellular parasite Neospora caninum, presents a significant challenge in veterinary medicine, leading to serious and life-threatening neurological issues in dogs, and costing the industrial cattle industry billions each year. N. caninum does not infect humans, making […]
Genomic deletions explain the generation of alternative BRAF isoforms conferring resistance to MAPK inhibitors in melanoma
Aya et al. show that the production of alternative BRAF mRNA isoforms (altBRAFs), associated with resistance to BRAF inhibitors in melanoma, is caused by genomic deletions rather than by alternative splicing, as previously thought. They also find that altBRAFs are present […]