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5 December 2013 11:26 am ,
Vol. 342 ,
Dyslexia, a learning disability that hinders reading, hasn't been associated with deficits in vision, hearing, or...
Exotic, elusive, and dangerous, snakes have fascinated humankind for millennia. They can be hard to find, yet their...
Researchers have sequenced and analyzed the first two snake genomes, which represent two evolutionary extremes. The...
Snake venoms are remarkably complex mixtures that can stun or kill prey within minutes. But more and more researchers...
At age 30, Dutch biologist Freek Vonk has built up a respectable career as a snake scientist. But in his home country,...
Since arriving on the island of Guam in the 1940s, the brown tree snake ( Boiga irregularis ) has extirpated native...
An animal rights group known as the Nonhuman Rights Project filed lawsuits in three New York courts this week in an...
Researchers have been hot on the trail of the elusive Denisovans, a type of ancient human known only by their DNA and...
- 5 December 2013 11:26 am , Vol. 342 , #6163
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DNA Damage Piles Up in the Aging Brain
9 June 2004 (All day)
Defective DNA has long been a suspect in the search for causes of impaired memory and learning. Now a comprehensive study of brain DNA provides solid evidence linking the culprit to the crime, which appears to be another woe of middle age.
A closer look at the crippled genes revealed damage caused by nasty free radicals, molecules that chew up DNA by the same process that turns metal to rust. Damage was most severe in the genes' promoter regions, the parts responsible for regulating when, and for how long, a gene is turned on. Compared to other sections of DNA, promoter regions are more vulnerable to attack from free radicals, and the cell can't repair them as well.
The results aren't all dismal though. The researchers also found that in older brains, activity was cranked up in genes that play a role in the body's immune response and combating stress and indicating that even if cells can't repair the damaged promoters, the brain tries to buffer the oxidative beating. And in human cells cultured in the lab, Yankner's team was able to repair much of the damage by artificially turning up the cell's DNA repair enzymes. While he cautions that the lab is a far cry from the brain, it raises the possibility that damage might be amenable to therapy in the future.
"The findings are really quite stunning," says neurologist Ann Graybiel of the Massachusetts Institute of Technology in Cambridge. "It gives new meaning to reaching 40."