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Thursday, September 27, 2012

Huntington disease gene carriers have quicker minds


Good news and bad news for people who carry the Huntington’s disease (HD) gene. The good news is that they apparently can learn more quickly than noncarriers. The bad news is that they have HD. Okay, I admit that’s not much of a trade-off. My apologies to anyone suffering from this fatal disease.

HD is caused by a dominant gene mutation. Thus, if one of your parents has the disease, you have a 50/50 chance of having it yourself. Nowadays, there is a genetic test that can tell whether a person has the mutation. Needless to say, choosing whether to get tested for an illness that is both inevitable and incurable is not an easy decision.

Christian Beste and his colleagues from Ruhr-Universitat Bochum and Leibniz Research Centre recruited participants who had made the choice to be tested. The researchers gave ‘pre-manifest’ HD gene mutation carriers (people who were as yet symptom free) and healthy controls a set of perception tests. The subjects were asked to detect changes in the brightness of bars on a screen. After the initial test, participants were given the opportunity to passively observe changes in brightness, a training method known to increase visual discrimination, and then retested. HD carriers improved as much with only 20 minutes of training as controls did after 40 minutes of training.

I’d like to delve into the world of utter speculation now. One reason that HD is as common as it is, affecting one of out every 10-20,000 people, is that most people have already reproduced by the time they realize they have the disease. Perhaps another reason is that being an HD carrier confers some cognitive advantage during the pre-symptomatic stage. Again, not much comfort to the unfortunates who will succumb to this illness, though this new knowledge may be of some use to people with other kinds of cognitive defects.


C
hristian Beste, Edmund Wascher, Hubert Dinse, & Carsten Saft (2012). Faster Perceptual Learning through Excitotoxic Neurodegeneration Current Biology DOI: 10.1016/j.cub.2012.08.012