Earlier this week a person of great interest passed away, leaving us with an inquisitive quote on death:
“No one wants to die. Even people who want to go to heaven don’t want to die to get there. And yet death is the destination we all share. No one has ever escaped it. And that is as it should be, because death is very likely the single best invention of Life. It is Life’s change agent. It clears out the old to make way for the new. Right now the new is you, but someday not too long from now, you will gradually become the old and be cleared away. Sorry to be so dramatic, but it is quite true.” –Steve Jobs
As scientists dive further into the workings of our body more becomes known. In today’s world some of the biggest questions revolve around prevention and reversal of diseases. As researchers work towards a full understanding of the brain, they sometimes stumble upon results leading to increased longevity. An example would be this week’s article in neurochemistry stating that the IGF1-R neuroreceptor in the brain might be a common causality of Alzheimer’s disease and aging of the brain. IGF1-R can lead a chain reaction that produces Aβ plaques which have long been believed to cause Alzheimer’s. On the other hand when IGF1-R is activated, it also creates a chain reaction that produces FOXO proteins which can lead to aging. This suggests that with some tweaking of IGF1-R pathways the length of a person’s life may be increased. Of caurse as I have mentioned in my previous blog post the body is extremely complicated and “tweaking” isn’t as easy as it sounds. Plus there are always bound to be side effects.
Yet even if we do begin to understand the chemistry of aging, is that something we want to modify? Just because a person can live longer doesn’t mean we live better. As chemistry begins to answer more difficult questions, it seems that ethical debates are likely to follow. I don’t know what the next 50 years holds, but I promise it will be interesting.
(1) Apfeld, J.; O’Connor, G.; McDonagh, T.; DiStefano, P. S.; Curtis, R. The AMP-activated protein kinase AAK-2 links energy levels and insulin-like signals to lifespan in C. elegans. Genes Dev 2004, 18, 3004-3009.
(2) Puglielli, L. Aging of the brain, neurotrophin signaling, and Alzheimer’s disease: Is IGF1-R the common culprit?. Neurobiol. Aging 2008, 29, 795-811.
