Eight years ago, U.S. scientists conducted a comparative genome analysis on centenarian siblings. The study revealed that among the hundreds of genes in the region of Chromosome 4, there was a gene or genes whose subtle modification could improve the odds of our living well beyond the average life expectancy. In an effort to uncover the physiological function of the CISD2 gene, which is located on the long arm of Chromosome 4, researchers from Taiwan’s National Yang-Ming University effectively linked CISD2 gene function, mitochondrial integrity and aging in mammals.
This discovery came when they engineered CISD2-deficient knock-out mice. By eight weeks, they observed signs of premature aging, including decreased body weight, loose skin, muscle atrophy, and lower subcutaneous fat deposition. Moreover, the researchers also discovered that the mouse’s normal two-year life span was cut in half when the CISD2 gene was disrupted.
As Dr. Tsai said in a press conference, the research program presented “a new animal model of human Wolfram Syndrome,” effectively linking the CISD2 gene function, mitochondrial integrity and aging in mammals. Wolfram Syndrome (WFS) is a rare, inherited neurodegenerative disorder primarily characterized by juvenile-onset diabetes, optic atrophy and premature death. Two categories of WFS (WFS1 and 2) are recognized, each with its own subset of variable symptoms, and resulting from mutations in the WFS1 and CISD2 genes, respectively. Additional research will be conducted to examine the utility of the CISD2 mouse model in order to understand WFS2 pathogenesis and explore the potential lifespan-extending effects of increased CISD2 expression.
News Release: Local scientists may have found secret of longevity www.taipeitimes.com May 16, 2009
News Release: Role for CISD2 gene in human disease and lifespan control www.sciencedaily.com
May 14, 2009
