Description

An ever-increasing fraction of the population reaches an age when - even in the absence of illness - physical and cognitive limitations affect quality of life. Aging induces characteristic changes in the brain (e.g. in the hippocampus) and the immune system (e.g. in T cells). Cells of both systems suffer from metabolic dysfunction as a result of a decline in the health of mitochondria - the powerhouses of cells - and reduced nutrient availability. Achieving more mechanistic insight into these changes will unveil new avenues leading to healthy aging. It was recently shown in cancer cells that inhibition of the cystine/glutamate antiporter system xc-, increases resilience against
glucose deprivation and improves mitochondrial health. Moreover, we discovered that mice lacking system xc-, have an increased lifespan and are protected against typical age-related impairments, including cognitive and immune dysfunction. We hypothesize that these beneficial effects of system xc- - deficiency are related to improved cellular metabolism. To test our hypothesis, we will 1/ establish the effect of genetic deletion of system xc- on age-related changes in the hippocampus- and T-cell-specific metabolic profile and 2/ gain cell- type specific mechanistic insight into the role of system xc- in modulating age-induced changes in mitochondrial function. The results of this study could unveil a novel strategy to counter
metabolic decline, an important focus in the development of
‘geroprotectors’
AcronymFWOAL968
StatusActive
Effective start/end date1/01/2031/12/23

    Flemish discipline codes

  • Adaptive immunology
  • Biogerontology
  • Cell physiology
  • Inflammation
  • Neurosciences not elsewhere classified

    Research areas

  • cystine, aging brain, immune system

ID: 49471306