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Archive - Jul 9, 2009


Crohn’s Disease Defect Associated with Poor Response to Mycobacteria

Approximately 25 perecent of patients with Crohn’s disease have a mutation in the NOD2 gene, but until now it has not been clear how this mutation might influence the disease. Now, researchers have obtained evidence that the NOD2 protein influences the binding of mycobacteria and the subsequent launching of an immune response. Defects in NOD2 can prevent binding of the mycobacteria and allow the establishment of persistent infections. The researches showed that the NOD2 protein preferentially recognizes a peptide called N-glycolyl-MDP, which is only found in mycobacteria. When mycobacteria invade the human body, they cause an immediate and very strong immune response via the NOD2 receptor. "Now that we have a better understanding of the normal role of NOD2, we think that a mutation in this gene prevents mycobacteria from being properly recognized by the immune system," explained Dr. Marcel Behr, senior author of the report. "If mycobacteria are not recognized, the body cannot effectively fight them off and then becomes persistently infected." This new discovery associates the predisposition for Crohn's disease with both the NOD2 mutation and the presence of mycobacteria, but researchers must still determine the precise combination of these factors to understand how the disease develops. The research was published online on July 6 in the Journal of Experimental Medicine. [Press release] [JEM abstract]

Caloric Restriction Extends Lifespan in Primates

A 20-year study in adult rhesus monkeys has shown that caloric restriction (CR) in these primates can extend healthy lifespan. At the end of the study, 37 percent of the control group had died of age-related causes, while only 13 percent of the CR group had. This finding means that the control monkeys experienced a death rate from age-related conditions such as diabetes, cancer, cardiovascular disease, and brain atrophy almost three times that of the CR group. Previous studies with yeast, worms, flies, and rodents have suggested that this kind of caloric restriction–a reduction of about 30 percent, and very different from malnutrition–can lead to such health benefits in some mammals, but given the many parallels between rhesus monkeys and humans, this study suggests that these benefits might occur in humans as well. "We have been able to show that caloric restriction can slow the aging process in a primate species," said Dr. Richard Weindruch, senior author of the study. "We observed that caloric restriction reduced the risk of developing an age-related disease by a factor of three and increased survival." The incidence of cancerous tumors and cardiovascular disease in animals on a restricted diet was less than half that seen in animals permitted to eat freely. Remarkably, while diabetes or impaired glucose regulation is common in monkeys that can eat all they want, it has yet to be observed in any animal on a restricted diet. "So far, we've seen the complete prevention of diabetes," said Dr. Weindruch. Furthermore, he noted, "The atrophy or loss of brain mass known to occur with aging is significantly attenuated in several regions of the brain. That's a completely new observation." The results of this study were published in the July 10 issue of Science.