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New research suggests possible treatments for diabetic neuropathy

September 4, 2012 in News

Diabetic neuropathy can cause a wide range of painful, troubling side effects – loss of sensation in hands or feet, trouble with digestion, trouble with regulating blood pressure, difficulties with sexual function, and even loss of bladder control. Close to half of all diabetics deal with one or more symptoms of diabetic neuropathy, which makes developing a greater understanding of the condition a priority for diabetes researchers.

Diabetic neuropathy can impact the peripheral nervous system, which is the part of the nervous system outside of the brain and spinal cord. The peripheral nervous system regulates almost every aspect of our bodily functions, including organ function. Nerves in the peripheral nervous system carry chemical “messages” between the brain and the rest of our body. If you reach out and touch a hot surface, messages from the brain through the peripheral nervous system allow your arm to move, and messages from receptors in your fingers travel back through the same system to allow you to recognize that the surface is hot.

In many ways, the nerves of the peripheral nervous system are like the electrical wiring in buildings. Like electrical wiring in your home, these nerves also have an insulating sheath that protects the underlying nerve. This insulation is called the “myelin sheath,” and is composed of Schwann cells.

What makes Schwann cells unique, and different from the plastic coating on the electrical wiring in your home, is that they can switch back and forth between two “forms.” Usually, they serve as a stable, protective coating. When a nerve is damaged, the cells can “demyelinate;” they switch to a ‘repair cell’ form and work to repair the damage.

While Schwann cells are remarkably good at repairing damage, they are not perfect. If the damage to the nerve is severe, or if something interferes with the Schwann cells, repairs can be incomplete, leading to long-term loss of function and pain.

High blood sugar can interfere with the body’s ability to bring oxygen to body tissues, including the Schwann cells. This can stress the cells and damage both the cells themselves and their ability to repair the nerves. Repeated cycles of switching forms can also stress and damage the cells. Over time, the impaired Schwann cells just cannot keep up with the wear and tear on the nerves that can occur due to high blood sugar.

Current research has focused heavily on the mechanisms that let Schwann cells switch back and forth to the repair cell form. If researchers can learn how to stimulate the repair cycle, it could offer help not only to patients with diabetic neuropathy, but also patients who suffer from a wide range of other conditions that damage the peripheral nervous system, or from severe trauma.

One team recently identified a protein, called cJun, that is a key factor in the ability of Schwann cells to take on their repair cell form. They also found a number of chemical pathways that activate cJun. One of these, called the p38 Mitogen Activated Protein Kinase Pathway, turned out to be especially important. This particular chemical pathway is activated when damage to the peripheral nervous system occurs, and may trigger the repair process.

Now that the research team has pinpointed some of the pathways that trigger nerve repair, they can start probing further; follow-up studies will focus heavily on how we may be able to manipulate this pathway with new treatments. This could lead to new medicines that could repair damage caused by diabetic neuropathy, or that reduce the damage diabetic neuropathy causes.

For more information about diabetic neuropathy, its symptoms, and possible treatments, you can read more on the American Diabetes Assocation’s website, or at the National Diabetes Information Clearinghouse. You can also read the original news release published in ScienceDaily for more information.

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