Crohn disease and ulcerative colitis represent the two common forms of idiopathic inflammatory bowel disease ( IBD ), each with a prevalence of roughly 100–150 per 100,000 individuals of European ancestry This week inNature Geneticsa "genome-wide association study of Crohn disease and two independent replication studies identify several new regions of association to Crohn disease."
This has been a disease that has multiple postulated causes. Some of the more modern include host-bacteria interaction leading to inflammation and disease. These associations implicate this as a possibility. More importantly they indicate risk of disease The genes are in addition to CARD15(NOD2) andIL23R.
A coding variant in ATG 16L1, the latter of which was also recently reported by another group is proven to be required for pathogenesis of Crohn's Disease. This gene is responsible for a process known asautophagy(required for our intrinsic immune system)
For non-scientsists /physicians
What does this mean? Well alot. If this is true, which it looks likely, then the next step is to clear the bowels(removing bacterium/Salmonella) of these persons with this polymoprhism. This would be another example of the possibility of personalized medicine. Treatment based on predisposition. I am sure there are alsopharma companies looking at halting ATG 16L12's function withRNA intereferenceas demonstrated in this study!
Crohn disease and ulcerative colitis represent the two common forms
of idiopathic inflammatory bowel disease ( IBD ), each with a prevalence
of roughly 100–150 per 100,000 individuals of European ancestry
This week inNature Geneticsa "genome-wide association study of Crohn disease
and two independent replication studies identify several new regions of association to Crohn disease."
This has been a disease that has multiple postulated causes. Some of the more modern include host-bacteria interaction leading to inflammation and disease. These associations implicate this as a possibility. More importantly they indicate risk of disease
The genes are in addition to CARD15(NOD2) andIL23R.
A coding variant in ATG 16L1, the latter of which was also recently reported by another group is proven to be required for pathogenesis of Crohn's Disease. This gene is responsible for a process known asautophagy(required for our intrinsic immune system)
For non-scientsists /physicians
What does this mean? Well alot. If this is true, which it looks likely, then the next step is to clear the bowels(removing bacterium/Salmonella) of these persons with this polymoprhism. This would be another example of the possibility of personalized medicine.
Treatment based on predisposition. I am sure there are alsopharma companies looking at halting ATG 16L12's function withRNA intereferenceas demonstrated in this study!