On Fri, 27 Aug 1999, Patrick Wilken wrote:
> FOR RELEASE: 26 AUGUST 1999 AT 14:00:00 ET US
> University of Wisconsin-Madison
> http://www.wisc.edu/
>
> Study details genetic basis of aging -- and how it might be delayed
>
> The Wisconsin team, led by Tomas A. Prolla, a UW-Madison professor of
> genetics, and Richard Weindruch,
I'm quite familiar with Dr. Weindruch, though not Dr. Prolla.
My first comment would be that I'm glad this work is being done because it will provide the concrete information to show that aging is really "treatable".
As a general comment I would say that the press release is a bit misleading (what do you want for a press release?).
Using gene-chips will only uncover "known" genes that may play a role in the aging process. It will not uncover the unknown regulatory factors that control those genes. An example of this would be recent evidence that leptin, the "hormone" produced by adipocytes (fat cells) is actually the sexual "maturation" hormone, i.e. it signals the brain that you have enough "resources" to reproduce and should become sexually mature. Now what we need is to know the maintenance and repair "hormones" that leptin may be down-regulating (if such exist) that switch you from "maintenence-and-repair" mode (i.e. a child or calorie-restricted individual) into a mature individual that ages.
As a second comment I would say that the idea is not novel. We extensively discussed this idea at Aeiveos Sciences Group for the differential display studies that I discussed at Extro 3. We even went so far as to contact several of the companies making the chips. The problems were that at that time (1996-7), the companies wanted very high prices "buy-in" ($500K+), and the genes required for a "mouse-chip" were to a large degree unknown.
Given the second comment it will be interesting to see if the patent they are applying for would be enforceable, since two of the main criteria for patents are that the be "novel" and "non-obvious".
Robert