New MSF Mailer - Part I

More news to be excited about!  This post (and the next post) contains information set forth in my latest MSF mailer.

First, interesting stuff about Myelin:

Myelin Influences How Brain Cells Send Signals

Myelin is well-known for its protective role in the central nervous system, but recent research suggests that myelin also plays a role in regulating a key protein involved in sending long-distance signals. The development of a new cell-culture system that mimics how specific nerve cell fibers in the brain become coated with protective myelin led to the discovery.

Ohio State University researchers have created a system in which two types of cells interact in a dish as they do in nature: neurons from the hippocampus and other brain cells, called oligodendrocytes, whose role is to wrap myelin around the axons.

MS has long been considered a disease of white matter, a reference to the white-colored bundles of myelin-coated axons that project from the main body of a brain cell. But researchers have discovered that the condition also affects myelinated axons scattered in gray matter that contains main bodies of brain cells, and specifically the hippocampus region, which is important for learning and memory.

Up to half of the people who have MS experience cognitive deficits in addition to physical symptoms. Researchers suspect that cognitive problems are caused by abnormal electrical activities of the demyelinated axons extending from hippocampal cells, but until now have not been able to test myelin's role in this part of the brain.

Now that the researchers can study how myelination is switched on and off for hippocampal neurons, they also can see how myelin does more than provide insulation – it also has a role in controlling nerve impulses traveling between distant parts of the nervous system. Identifying this mechanism when myelin is present will help improve understanding of what happens when axons in this critical area of the brain lose myelin as a result of MS, researchers say.

 Second, bone health is important and more about vitamin D:

Bone Health a Factor in Early MS

Osteoporosis and low bone density are common in people in the early stages of MS, according to a new study.
“We’ve known that people who have had MS for a long time are at a greater risk of low bone density and broken bones, but we didn’t know whether this was happening soon after the onset of MS and if it was caused by factors such as their lack of exercise due to lack of mobility, or their medications or reduced vitamin D from lack of sun exposure,” said study author Stine Marit Moen, M.D., of Oslo University Hospital Ulleval in Norway.
Low vitamin D levels are associated with an increased risk of MS. Low vitamin D levels can lead to reduced calcium absorption and bone mineralization, or the process the body uses to turn minerals into bone structure.
“Our hypothesis was that if vitamin D exerts a major effect on the risk of MS, then the effects of low vitamin D levels on bone density would be apparent soon after the onset of MS,” Moen said.
The study involved 99 people with an average age of 37 who were recently diagnosed with MS or clinically isolated syndrome, which means they had a first episode of symptoms like those in MS but have not yet been diagnosed with the disease. All had no or minor physical disability from the disease.
The participants had bone density tests an average of 1.6 years after the first time they had any symptoms suggestive of MS. Their tests were compared to bone tests of 159 people of similar age, gender, and ethnicity who did not have the disease.
A total of 51 percent of those with MS had either osteoporosis or osteopenia, compared to 37 percent of those who did not have the disease. Osteoporosis is a disease where low bone density causes the bones to become thin and brittle, making them more likely to break. Osteopenia is low bone density that is less severe than osteoporosis but puts a person at risk for osteoporosis.
The results remained the same after researchers adjusted for other factors that can affect bone density, such as smoking, alcohol use, and hormone treatment.
“These results suggest that people in the early stages of MS and their doctors need to consider steps to prevent osteoporosis and maintain good bone health,” Moen said. “This could include changing their diet to ensure adequate vitamin D and calcium levels, starting or increasing weight-bearing activities and taking medications.”

The study was published in Neurology, the medical journal of the American Academy of Neurology.

Third, more on understanding MS:
 

MS-Like Disease in Monkeys may Yield Helpful Clues 

The discovery of a naturally occurring disease in monkeys that is very much like MS in humans could have a major impact on efforts to understand the cause of the disease. The disease that researchers from Oregon Health & Science University (OHSU) discovered in monkeys at the Oregon National Primate Research Center is associated with a herpes virus that could give significant clues into how MS develops in humans. MS researchers have long believed that a type of herpes virus may trigger multiple sclerosis in people who are genetically susceptible to the disease.  

"These findings could have a huge impact on our understanding of MS and could be a landmark in someday developing more effective treatments for the disease, or even methods to prevent the onset of MS," said Scott Wong, Ph.D., senior author of the study and a scientist at the Vaccine and Gene Therapy Institute and the Oregon National Primate Research Center.
Before the OHSU findings, researchers had been able to study MS-like diseases in nonhuman primates only after the disease had been artificially induced. A naturally occurring disease, such as the one discovered at OHSU, can give researchers many more clues into the causes and development of the disease.
"Now, we may be able to tease apart what's triggering the onset of the disease," Wong said.
And the fact that the disease, found in a small percentage of the Japanese macaques at OHSU each year, came from a herpes virus could prove hugely important to MS researchers worldwide. Researchers can now search for a similar virus in people with MS.
From 1986 through 2010, 56 of the Japanese macaque monkeys at the Oregon National Primate Research Center at OHSU spontaneously developed paralysis in their hind limbs, along with other symptoms. The monkeys were humanely euthanized because they could not have been returned to the monkey colony safely. Researchers later did necropsies on their bodies and performed MRI scans on eight of the animals.
That work and other testing allowed researchers to discover that an MS-like disease called Japanese macaque encephalomyelitis was causing the paralysis. While the disease typically afflicted young adult animals, it also was present in juveniles and older animals, and was present in both males and females.
About 1 to 3 percent of the more than 300 Japanese macaques at the primate center develop the disease each year, according to the researchers.
With this discovery, MS researchers now will be able to move toward trying to prevent or treat the virus in monkeys, which might help scientists make progress in treating MS in humans. The OHSU researchers' findings were published online in the Annals of Neurology.

Always nice to know that they have found a possible cause of MS - maybe a virus is to blame!

Axon Damage Might Precede Myelin Damage?

An article from an MS Foundation mailer that I received:

Axon Damage May Precede Myelin Damage
It has recently been discovered that axons, or nerve cells, can start degenerating spontaneously without prior damage to their protective myelin coating. If found and treated early, this process can be reversed in mice, which may lead to new effective treatments for MS, according to the findings of a study published in Nature Medicine.

In the paper, senior authors professor Martin Kerschensteiner of the Ludwig-Maximilians-Universität in Munich, Germany, and professor Thomas Misgeld from the Technical University of Munich, and colleagues describe how they found a previously unknown type of axon or nerve cell degeneration, which they call "focal axonal degeneration" (FAD).

While the discovery opens the door to new drug targets, the researchers warn there is still a lot of work to be done before effective treatments are available, as Kerschensteiner explained:

"As yet, we only have a superficial understanding of the underlying molecular mechanisms and, of course, finding effective therapies will require time-consuming screens and extensive trials of drug candidates," he cautioned.

Autoimmune diseases like MS occur when the immune system, which normally only targets and destroys foreign agents such as toxins, bacteria and viruses, that have entered the body, instead attacks the body's own tissue, causing inflammation and eventually degeneration of the area affected.

The predominant view is that axon damage in MS follows the gradual destruction of the myelin sheath, the protective, electrically insulating coating of tissue surrounding the axon that speeds up the transmission of signals.

What triggers the axon damage itself, however, is poorly understood, and it was this that Kerschensteiner and Misgeld were trying to learn more about using lab mice when they made their surprising finding.

The finding may explain why some patients with MS experience spontaneous remission of symptoms:

"In its early stages, axonal damage is spontaneously reversible," said Kerschensteiner. "This finding gives us a better understanding of the disease, but it may also point to a new route to therapy, as processes that are in principle reversible should be more susceptible to treatment."

“However, before any potential drugs can even be considered, never mind put forward for trial, we need a much better understanding of the underlying molecular chemistry and biology of a disease.”

Previous studies of MS have already suggested that reactive oxygen and nitrogen radicals, chemicals produced by the immune system, play an important part in destroying axons. The researchers suggest in the case of FAD, these aggressive chemicals attack the mitochondria inside the nerve cells. Mitochondria are the "power cells" inside cells, they synthesize ATP molecules, the universal "currency units of energy" with which cells build, maintain and operate themselves.

In the lab mice, they were able to take action to rescue axons that had already started degenerating.

And in a final stage of their study, they found characteristic signs consistent with FAD in brain tissue from humans with MS, giving hope that the same treatment principles they established in the mice might also work in humans.

I find this to be VERY interesting, considering the fact that I have only ever been told that MS is the result of the immune system attacking the myelin, thus damaging the body's ability to properly transmit the neurons.  It is very intriguing to now learn that the axons may be damaged without damage to the myelin sheath!  I cannot wait to learn more about this research!