Sunday, November 20, 2005


Want to live forever?

The day when that is possible is not too far off. Are we ready? I thought I might summarize a bit of recreational reading for the weekend, volume 1019 of the New York Academy of Sciences, Strategies for Engineered Negligible Senescence . NYAS is one of the best place to learn about medical scientific trends. In my humble opinion, of course. I'll spare you the technical details, many of which I am not competent to discuss anyway. There are many articles in this 592 page volume that I didn't read, so don't feel as if I've given away the ending. But here's a brief dip. The book is organized mostly by organ system, with the brain getting top billing and the cardiovascular system next. But oxidative stress gets ca. 70 pages and protein and DNA damage figure prominently, too, as does cancer. The Nervous System * Is amyloid plaque what causes Alzheimers, or is it a protective anti-oxidant response? (my opinion, which is worth at least twice as much as the electrons this page is printed on, is that it is the latter.) * Instead of using stem cells to replace lost tissues, how about using them to manufacture from glial cell growth factor to protect neurons? * Cold sores cause brain sores. Herpes simplex is statistically associated with Alzheimer's in people with a specific allele of the gene for apolipoprotein E. * Aging affects mitochondrial competence in handling calcium in neurons. Mitochondria are heterogeneous in both size and competency. In rats, this does not seem to be age related, at least as measured in cytochrome oxidase positive synaptic mitochondria. * Women are three years ahead of men in developing Alzheimer's (the gross oversimplification in this statement is mine, not the author's) * Could Vitamin E deficiency cause premature aging? It may affect the production of a protein called MAP-2 that may affect growth, differentiation, and plasticity of neurons. It does not affect GAP-43, a protein associated with development, learning, and regeneration. In rats. In the "cerebeller cotex" (double sic). * Cytidine phosphocholine seems to act as a neuroprotector, causing an increase in astrocytes and a decrease in NADPH-d neurons, from which we can conclude that authors who fail to spell out all abbreviations should be shot and not hanged (NADPH-d is NADPH-diaphorase, an activity associated with the production of nitric oxide). * Does aluminum cause Alzheimer's, perhaps through oxidative stress? Elderly male Wistar rats say yes. The concentration of aluminum increases in the prosencephalon + mesencephalon (PME) and pons medulla. The PME and PMD also picked up copper, zinc, and manganese. The mossy fibers of the hippocampal C3 subfield were enlarged. The authors propose that metals destabilize cell membranes and facilitate oxidative stress. * Play with your rat to keep it from becoming senile. Potential human implications: give grandma new toys for Christmas, ideally from Lamborghi or Silicon Graphics. * From authors at Max Planck Institute, the Institute of Management Problems, and Duke University: Some of the herbals and several commercial antidepressants may have beneficial effects. These incldue improved learning, memory, brain metabolism, and capacity, reduce oxidative stress damage, and even regenerate brain. Some of these include gamma amino butyric acid, piracetam, gingko biloba, deprenyl, trental (pentoxyphilline, hydergine, estrogen, aspirin, and Vitamin E. Before rushing out any buying any of these, you might want to read the fine print. Like, aspirin and gingko's effects are evident only in very elderly cohorts. Vitamin E may worsen infections in the elderly. Vitamin A good, iron bad (but results not in publishable form yet). And so on. I'll try to cover other topics from this fascinating book as time permits.
Check out Tales of the X-Mice over at Pharyngula. We already have mutant mice that can regenerate heart tissue. Next step: Neurons. Once that hurdle's cleared, immortality is not far off.
Interesting read. As the man says, "The bad news? At least 20 different genes are involved in the regeneration ability of the MRL mouse. This is a very complex characteristic, not one we're going to figure out how to turn on in ourselves next week."

What those genes represent is presumably some combination of proteins that either promote growth and remodeling, like MAP-2, or can produce substances like NADPH-d which are involved in the production of nitric oxide.

But even if we were somehow to find the MRL equivalent for human beings, that's not enough. MRL mice regenerate, but it's not clear that regeneration is what's wanted. Protection is what is best.

And then there's telomeres.

But each baby step toward knowledge, repeated many times over the course of years brings great changes in medicine.
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