An ever-increasing fraction of the population reaches an age when, even in the absence of illness, physical limitations affect quality of life. Aging is accompanied by characteristic changes in e.g. the brain and the immune system, which are known to bi-directionally communicate. Achieving more mechanistic insight into these
changes might unveil new avenues leading to healthy aging. We discovered that mice lacking the cystine/glutamate antiporter system xc-, have an increased lifespan and are protected against typical
age-related impairments, including cognitive and immune dysfunction. To test our hypothesis that these beneficial effects arise from the absence of system xc- on immune cells rather than the brain, we perform bone marrow transplantations to manipulate the expression of system xc- only in the cells of the peripheral immune system, and study the effect on the aging process. Next, we further investigate the therapeutic potential of system xc- inhibition in age- related neurological disorders: we study the effect of system xc- - deficiency in a mouse model for Parkinson’s disease (PD; treatment of aged system xc- - deficient mice with a PD-inducing toxin) and Alzheimer’s disease (AD; cross-breeding of system xc- - deficient
mice with a genetic mouse model for AD). Confirming the therapeutic potential of system xc- in age-related disorders, together with mechanistic insight could simplify and accelerate the search for therapeutic strategies that target system xc-.
Effective start/end date1/11/1931/10/21

    Flemish discipline codes

  • Biogerontology
  • Inflammation
  • Cognitive neuroscience
  • Neurological and neuromuscular diseases
  • Electrophysiology

    Research areas

  • system xc-, Aging, hippocampla function

ID: 47878803