Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a disease in which the neurons that control voluntary muscles die. Typical symptoms include stiff muscles and muscle twitching. Patients may have difficulties with speaking, swallowing and even breathing.
Increased levels of the IP3R2 protein has been found in the bloodstream of many ALS patients. It is thought that reducing ALS expression may be a way to protect the damaged motor neurons. However, what a new study finds is opposite to that hypothesis.
VIB scientists discovered that IP3R2 actually protects against inflammation in ALS. In addition, this mechanism may exist not only in ALS but also in other disorders. The finding has been reported in Human Molecular Genetics.
There is no cure for ALS now. This disease affects about 2.7 people per 100,000 each year in Europe. Some cases are due to mutations in a gene that produces superoxide dismutase 1 (SOD1). The researchers used a mouse model of this form of ALS in the study.
In mouse models of ALS, the expression of IP3R2 is elevated. After the researchers deleted the IP3R2 gene in mouse models, the animals died sooner. In addition, they observed systemic inflammation and higher levels of some molecules which are involved in the immune response. Based on these results, the researchers believed that elevating the IP3R2 level may be a protective response.
Now, the research team are investigate cells from skin fibroblasts of ALS patients to see whether there are changes in calcium metabolism. Understanding the role of IP3R2 in ALS could help to improve the treatment of the disease. The researchers noted that inflammation to some extent could paly a role in ALS. But more research is needed to understand the molecular mechanism of it.
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