Kári Stefánsson has served as President, Chief Executive Officer and Director since he co-founded deCODE in August 1996. Dr. Stefánsson was appointed to serve as the Chairman of the company's Board of Directors in December 1999. From 1993 until April 1997, Dr. Stefansson was a professor of Neurology, Neuropathology and Neuroscience at Harvard University. In addition, from 1993 through December 1996 he was Director of Neuropathology at Beth Israel Hospital in Boston, Massachusetts. From 1983 to 1993, he held faculty positions in Neurology, Neuropathology and Neurosciences at the University of Chicago. Dr. Stefansson received his M.D. and Dr.Med. from the University of Iceland.
Genetics of longevity in Iceland
In their studies of the genetics of common diseases, scientists at deCODE genetics have collected a formidable amount of both phenotypic and genotypic data on more than 50% of the adult population of Iceland. When these data are analyzed in the context of data on the genealogy of the entire Icelandic nation it provides considerable transparency into the genetics of the lifespan of people. I will discuss the following observations on the genetics of longevity that we have extracted from these data:
- In Iceland there is considerable genetic component to the risk of becoming more than 90 years of age. The effect of this begins to show once an individual becomes 65 years of age; those who have at least one parent who becomes more than 90 stand a significantly less change of dying within a year than those with both parents dead at less than 90. Furthermore, the genetic component of longevity appears to be relatively simple.
- We have mapped to genomewide significance two genes that confer increased risk of longevity in Iceland.
- In one of the longevity loci we have found an inversion of approximately 0.9 Mb that is significantly associated with longevity in Iceland. Within the inverted segment of DNA there are several genes in which expression is influenced by the orientation of the inverted piece. Variants in one of them have previously been implicated in deterioration of cognitive function.
- The second longevity locus coincides exactly with a locus that contains a gene that influences the expression of another gene that contains variants some of which predispose Alzheimer’s Disease and others that protect against the same.
Our conclusions are that:
- The risk of becoming 90 years of age has a genetic component that is significant enough to reach through a long life of environmental influences.
- The genetic component is simple enough to lend itself to analysis with linkage.
- It appears that the integrity of the brain is one of the factors that cap our lifespan potential.