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Mars mission Risk 29: Scientists research ways to reduce radiation-induced brain damage

irment results solely from the death of the brain's neurons. Britten believes other, more complex mechanisms are at work, processes that could be manipulated by NASA's medical staff.

"Once we understand what's not working, then maybe we can fix it," said Britten.

Because radiation damage is similar to the free-radical injury resulting from aging and other neurological diseases, the research could lead to better treatments for conditions like Alzheimer's disease that cause progressive dementia.

The projects of the twelve teams investigating the cosmic radiation risks, listed by principal investigator, are:

  • Edouard Azzam, University of Medicine and Dentistry of New Jersey, Newark, N.J., the role of gap-junction communication and oxidative metabolism in the biological effects of space radiation

  • Susan Bailey, Colorado State University, Fort Collins, Colo., telomeric proteins in the radiation/DNA damage response

  • Richard Britten, Eastern Virginia Medical School, Norfolk, Va., proteomic aided investigation of the mechanistic basis for HZE-induced cognitive impairment and the development of diagnostic biomarkers

  • David Chen, University of Texas Southwestern Medical Center, Dallas, mechanisms of the repair of HZE-induced DNA double-strand breaks in human cells

  • Albert Fornace, Harvard School of Public Health, Boston, mouse models approach for intestinal tumorigenesis estimates by space radiation

  • Kathryn Held, Massachusetts General Hospital, Boston, mechanisms for induction of bystander effects by high energy particles in cells and tissues

  • Fiorenza Ianzini, University of Iowa, Iowa City, Iowa, role of high-LET radiation-induced mitotic catastrophe in mutagenesis: implication for carcinogenesis

  • Amy Kronenberg, Lawrence Berkeley National Laboratory, Berkeley, Calif., comparative analysis of charged particle-induced autosomal mutations in murin
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Source:Eastern Virginia Medical School


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