Nicotine May Improve MS Symptoms, Research in Mice Demonstrates

We know that cigarette smoking is bad for our health. The Centers for Disease Control and Prevention (CDC) states that more than 16 million Americans suffer from a disease caused by smoking, such as cancer, heart disease, stroke, lung diseases, or diabetes. In the United States, cigarette smoking is responsible for more than 480,000 deaths per year, including an estimated 41,000 deaths in persons exposed to secondhand smoke. Worldwide, tobacco use kills more than 5 million people annually with numbers growing each year.

Epidemiological studies have reported that cigarette smoking increases the risk of developing multiple sclerosis and accelerates disease progression (Sundstrom, 2008). A recent study demonstrated that in a large population of MS patients in England, current smoking behavior was associated with more than 2.5-fold increased risk of death. In addition, the life expectancy of current smokers with MS was reduced by about 10 years as compared to non-smokers with MS (Manouchehrinia, 2014).

It is logical that smokers who understand the increased risk of tobacco would want to do what they can to limit their exposure to nicotine or other harmful chemicals while smoking. Hence the tobacco industry has developed “reduced exposure” or “light” products containing lower levels of nicotine, nitrosamines, or other chemicals deemed to be potentially toxic. However, these ultralow nicotine or tobacco-free cigarettes may be worse than their full flavor versions.

Researchers comparing the effects of exposure to full flavor, nicotine-free, or ultralow nicotine products on the integrity of the blood-brain-barrier (BBB) found that nicotine-free and ultralow nicotine cigarettes are potentially more harmful to the BBB endothelium than regular tobacco products. This study demonstrates that the detrimental effect of tobacco smoke on the BBB is strongly correlated to the tar and nitric oxide levels in the cigarettes rather than the nicotine content (Naik, 2014).

Meanwhile, a different team of researchers have assessed the effects of nicotine and non-nicotine components of cigarette smoke on experimental autoimmune encephalomyelitis (EAE), a form of MS induced in mice. They found that nicotine significantly improved the severity of EAE, as shown by reduced demyelination, increased body weight, and attenuated microglial activation. Nicotine administration after the development of EAE symptoms prevented further disease exacerbation, suggesting that it might be useful as an EAE/MS therapeutic agent (Gao, 2014).

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Could Nicotine Be Used to Treat MS Someday?

Human Stem Cells Help Mice Regain Mobility

Researchers at the University of California stumbled upon an unexpected outcome while studying the common problem of stem cell rejection following transplantation.  Scientists injected human neural precursor cells (hNPCs) derived from human embryonic stem cells (hESCs) into the spinal cords of mice infected with the neurotropic JHM strain of mouse hepatitis virus (JMHV) http://www.ncbi.nlm.nih.gov/pubmed/11935460 .  Persistent infection with this particular virus causes an MS-like condition in mice characterized by demyelination, neuroinflammation, and hind-limb paralysis. 

As expected, the stem cells injected into the JHMV-infected mice were completely rejected by the immune system within 8 days.  However, unexpectedly, the hNPC-transplanted mice experienced improved motor skills and a reduction in neuroinflammation and demyelination about two weeks after the injections.  Results of a follow-up study cofunded by the National MS Society and the California Institute for Regenerative Medicine are published in the journal Stem Cell Reports in the article, “Human Neural Precursor Cells Promote Neurologic Recovery in a Viral Model of Multiple Sclerosis.”

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Mice with MS-like Disease Unexpectedly Walk After Stem Cell Transplantation

Modeling MS in Mice to Study Remyelination

To investigate potential causes and treatments for demyelinating diseases such as MS, researchers use various methods to cause a condition or symptoms similar to MS in laboratory animals.  Mice do not naturally develop MS, but mice are especially suited to studying MS-like disease because of their similarity to humans in anatomy, physiology, and genetics.  Researchers are able to create various genetic modifications in mice to mimic human disease.  Mice are small, inexpensive, and can reproduce quickly.

There are three major types of animal models used to study demyelinating disease: 1) genetic models, where genes important for CNS myelination, myelin maintenance or glial function have been altered; 2) immune-mediated models of induced pathogenesis towards myelin; and 3) toxin-mediated models using toxic substances that preferentially affect myelin (Pohl, 2011).
- See more at: http://www.healthcentral.com/multiple-sclerosis/c/19065/169331/sclerosis-disease#sthash.WodvrOeA.dpuf

To investigate potential causes and treatments for demyelinating diseases such as MS, researchers use various methods to cause a condition or symptoms similar to MS in laboratory animals.  Mice do not naturally develop MS, but mice are especially suited to studying MS-like disease because of their similarity to humans in anatomy, physiology, and genetics.  Researchers are able to create various genetic modifications in mice to mimic human disease.  Mice are small, inexpensive, and can reproduce quickly. 

There are three major types of animal models used to study demyelinating disease: 1) genetic models, where genes important for CNS myelination, myelin maintenance or glial function have been altered; 2) immune-mediated models of induced pathogenesis towards myelin; and 3) toxin-mediated models using toxic substances that preferentially affect myelin (Pohl, 2011).

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Multiple Sclerosis Research: Studying MS-like Disease in Mice