Slow brain repair seen in Huntington’s

From Orlando, Fla., at a meeting of the Society for Neuroscience

The human brain may struggle heroically, but in vain, to replace the nerve cells that die in Huntington’s disease, a New Zealand research team suggests.

Over the past few years, neuroscientists have been surprised to find that healthy, adult mammalian brains generate new nerve cells from so-called stem cells residing in select regions of the brain. It’s unclear how important this ongoing neurogenesis is, but some researchers have linked it to memory storage and other brain functions.

By studying the brains of people who died with Huntington’s disease, Maurice A. Curtis of the University of Auckland in New Zealand and his colleagues have shown for the first time that neurogenesis also occurs during the course of this fatal disorder. Curtis’ group found evidence of a protein called proliferating cell nuclear antigen (PCNA), which marks dividing cells, and a protein called class III beta-tubulin, which is specific to new nerve cells.

Moreover, the pace of neurogenesis seemed to correlate with the severity of a person’s disease at death: The brains of people worst afflicted with Huntington’s showed the most PCNA.

Apparently, says Curtis, brains besieged by Huntington’s can’t generate new nerve cells fast enough to replace the dying ones. Or perhaps the new cells can’t migrate to the damaged sites where they’re needed. Ultimately, scientists aim to find ways of boosting the brain’s own repair processes to counter Huntington’s and related diseases, says Curtis.


If you have a comment on this article that you would like considered for publication in Science News, please send it to

More Stories from Science News on Health & Medicine