Multiomics identify the gene expression signature of the spinal cord during aging process

This study investigates the aging process in the spinal cord by examining gene expression changes. Using advanced techniques like spatial transcriptomics and RNA sequencing, researchers compared young and aged spinal cords to identify key genes and pathways involved in senescence. The research highlights the role of a gene called Fth1, which is associated with ferroptosis (a form of cell death). They found that Fth1 is upregulated in aged spinal cords, making cells more resistant to ferroptosis, a process that could contribute to age-related decline. The findings suggest that resistance to ferroptosis could be a significant characteristic of aging, not just in the spinal cord but potentially in other tissues as well. This could open new avenues for developing treatments to combat age-related disabilities.

• 1
  Bulk RNA sequencing identified 526 upregulated genes and 300 downregulated genes in senescent spinal cords compared to young spinal cords, with pathways related to phagosome function, neuroinflammation, ferroptosis, and necroptosis being enriched.
• 2
  Spatial transcriptomics revealed distinct neuronal and glial subtypes in young and senescent spinal cords, and showed that the ferroptosis-associated gene Fth1 is upregulated in aged spinal cords.
• 3
  In vitro experiments demonstrated that senescent mixed glial cells are resistant to ferroptosis, and that overexpression of Fth1 in normal mixed glial cells reduces their sensitivity to ferroptosis, while Fth1 knockdown increases their sensitivity.