Recent Studies Associate Protein Levels with Myositis

Recent studies by the Department of Neurosciences, Psychiatry and Anesthesiology from AOU “G. Martino”, Messina, Italy came up with observations that may help further understand the nature of myositis.

Myositis is a rare disease characterized by progressive muscle inflammation, weakening and atrophy. Because of its rarity – and because the onset is generally gradual and may involve different muscles from the trunk to the extremities – it is very easily misdiagnosed. The usual victims are from the age 50 and above, although some cases are found in younger patients. It occurs more in men than in women.

In the said study, doctors investigated the behavior of two proteins – ANT1 and NF-kB – in Inclusion Body Myositis or IBM, and in Polimyositis or PM. After analyzing muscle samples from five patients and subjecting these to immunocytochemistry, they found that ANT1 are lower in IBM samples compared to those of PM and in controlled NF-kB.

The proponents of the study suggests that the reduction of ANT1 coupled with the over-expression of NF-kB may explain the lack of apoptosis in myositis. (Apoptosis, as you may know, is the cell’s process of self-destruction or degeneration, mostly believed to be programmed instructions from the genes itself to produce certain proteins that trigger the process of cell death in many diseases.) The study concurs with previous findings from those conducted by USC’s Department of Neurology that “NF-kB plays a role in IBM pathogenesis.” That report published in September 1998 said that “different distributions of NF-kB subunits in necrotic fibers and at normal neuromuscular junctions (NMJs) suggests different roles of each subunit in human muscle pathology and physiology.”

Meanwhile, the most recent report from AOU also stated normal ANT1 expression in PM could be related to the scarcity of mitochondrial abnormalities in the disease. But it could also suggest that these two conditions – the reduction of ANT1 and the increase of NF-kB – diverge in activating different anti-apoptotic pathways. Whichever is the case, both observations invite questions as to the role of NF-kB in cell-degeneration: Could it be that NF-kB is the gene’s signal to start the process of cell degeneration? Or is it the case of the egg that came from the chicken and that NF-kB is just a product of the process? Will the study on ANT1 hold the key to fighting myositis in all its forms?

As for patients, how is this information of help? First, there really is still a lot to learn about the disease. It helps to know that dedicated doctors and scientists are not letting up on getting more understanding of myostatis. Second, it gives hope that studies on myositis are slowly but surely gaining headway. Soon we may have a clearer understanding of how myositis begins and therefore find the way to prevent it.