Opening

Opportunity Structures: A Research Note on the Epigenetics of Alzheimers Disease by

Richard M. Hessler

Since 1993, I have been working with colleagues in Sweden on a longitudinal study of aging. It
is named H70 and is housed in the Department of Geriatric Medicine, Gteborg University,
under the direction of Ingmar Skoog, Professor of Geriatric Medicine.

http://agecap.gu.se/english/research

Much of the research I have been part of pointed to social networks as a significant predictor of
higher odds of living longer and healthier if social networks were more extensive and intensive
than if not. Also, we found that people who had strong networks and lived long healthy lives
had shorter periods of morbidity in the last year of life compared to shorter lived people. Living
longer may not be a socio-economic burden as often portrayed in the media.

Now we are focusing on chronic diseases, specifically Alzheimers. We realize that this chronic
disease, along with others, exacts a terrible toll on the socio-cultural integrity of societies the
world over, mainly through the burdens of expensive protracted care and the devastating loss
of social self among the victims. Such a disease surely must affect the opportunity structure
adversely.

The H70 study is a gold mine for researchers interested in early detection of Alzheimers,
factors involved in its genesis, and ultimately its prevention. Part of H70s potential in this
regard is due to the research design: every respondent age 70 at the start; several data
gathering points during the 30-year study period; data collected on more than 2,000 biopsycho-social variables; and blood samples frozen in anticipation of cracking the human
genome.

We think that Alzheimers disease that strikes after age 70 is unlike Alzheimers that starts at
age 40 in that the genetic mutation that drives the latter seems to inevitably lead to the onset
of the disease whereas the late onset version of the disease seems to have a mutation that
exists in some people who never show symptoms. That is the idea a suppressor nucleotide
within messenger RNA that keeps the mutation from fully expressing itself and does so until
something damages the suppressor and turns on the bad gene.

We extracted the DNA from the frozen blood samples and are doing a pilot study on 100 cases
of only women, 50 who died with the diagnosis of Alzheimers disease, and 50 others, matched
on social networks, smoking, and depression, who did not die with the diagnosis of Alzheimers.
Our goals are simple: 1. Find the biomarker or mutation that would allow for early detection;
2. Test drive the bioinformatics behind the analysis; 3. See if the mutation is acquired during
the study period; and 4. Iron out problems in cross cultural teamwork that might arise.