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    You are here : Home » MS Research News » Lipids And MS

    Lipids And MS

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    More news can be found in New Pathways Magazine, our bi-monthly publication, and also check daily at MSRC: Latest MS News.

    Replacing fatty acids may fight MS

    LipidsBy delving into the components of protective nerve coatings that get damaged in multiple sclerosis, scientists have identified a handful of lipid molecules that appear to be attacked by an immune system run amok.

    Bolstering the supply of these lipids might help preserve these nerve coatings and, in the process, knock back the inflammation that contributes to their destruction, researchers report in the June 6 Science Translational Medicine.

    In MS patients, rogue antibodies assault myelin, the fatty sheath that insulates nerves and facilitates signaling. Inflammation exacerbates the attack on myelin and the cells that make it. But other details of MS, including the roles of myelin lipids, have been less clearly understood.

    “I think this is a very good study,” says Francisco Quintana, an immunologist at Harvard Medical School. “Overall, there are not many papers on lipids in MS. Technically, they are challenging and require a lot of expertise.”

    To explore the role of lipids, the researchers studied spinal fluid from people with MS, healthy people and patients with other neurological disorders. Tests on the fluid showed that antibodies targeted four lipids more often in MS patients than in the other groups. Examination of autopsied brains from MS patients and people without MS revealed that, in the MS patients, these four lipids were depleted at the sites where the nerve coatings were damaged.

    A nerve needs an intact myelin sheath to conduct signals. “It short-circuits if they are not there,” says study coauthor Lawrence Steinman, a neurologist at Stanford University. This nerve damage causes loss of muscle control and other symptoms characteristic of MS.

    Steinman and his colleagues conducted tests in mice with a condition similar to MS and found that injections of the lipids over several weeks could limit severity of the disease and even reverse some symptoms in the animals. The four lipids — abbreviated as PGPC, azPC, azPC ester and POPS — share a similar phosphate group, to which the rogue antibodies bind.

    Other tests in mice showed that side chains of fatty acids, attached to the lipids like fingers on a glove, “keep the myelin-making cells alive and reduce the inflammatory response,” Steinman says. “It turns out that the side chains are imbued with protective properties.” They repel inflammation and even kill the T cells that trigger it, the researchers found.

    It could be that people with MS, who lack adequate supplies of these lipids and their protective fatty acids, fail to keep up with the destruction caused by antibodies and inflammation. But that dismal numbers game might present an opening for future research, Steinman says. Just as the mice benefited from receiving extra lipids, human patients might, too. And some tests now show that mice can take the lipids orally and still improve, he adds.

    Quintana says that further animal studies will be needed to clarify the full effects of giving lipids to fight MS. “But it could potentially lead to some kind of therapy.”

    Joan Goverman, an immunologist at the University of Washington in Seattle, says the researchers deserve credit for their approach. “Looking at humans and then going back and incorporating that in animal models is a powerful way to understand the disease.”

    Source: Science News © Society for Science & the Public 2000 - 2012 (07/06/12)

    Multiple Sclerosis not disease of immune system?

    MS DiagnosisAn article to be published Friday (Dec. 23) in the December 2011 issue of The Quarterly Review of Biology argues that multiple sclerosis, long viewed as primarily an autoimmune disease, is not actually a disease of the immune system.

    Dr. Angelique Corthals, a forensic anthropologist and professor at the John Jay College of Criminal Justice in New York, suggests instead that MS is caused by faulty lipid metabolism, in many ways more similar to coronary atherosclerosis (hardening of the arteries) than to other autoimmune diseases.

    Framing MS as a metabolic disorder helps to explain many puzzling aspects of the disease, particularly why it strikes women more than men and why cases are on the rise worldwide, Corthals says. She believes this new framework could help guide researchers toward new treatments and ultimately a cure for the disease.

    Multiple sclerosis affects at least 2.5 million people worldwide. Its main characteristic is inflammation followed by scarring of tissue called myelin, which insulates nerve tissue in the brain and spinal cord. Over time, this scarring can lead to profound neurological damage. Medical researchers have theorized that a runaway immune system is at fault, but no one has been able to fully explain what triggers the onset of the disease. Genes, diet, pathogens, and vitamin D deficiency have all been linked to MS, but evidence for these risk factors is inconsistent and even contradictory, frustrating researchers in their search for effective treatment.

    “Each time a genetic risk factor has shown a significant increase in MS risk in one population, it has been found to be unimportant in another,” Corthals said. “Pathogens like Epstein-Barr virus have been implicated, but there’s no explanation for why genetically similar populations with similar pathogen loads have drastically different rates of disease. The search for MS triggers in the context of autoimmunity simply hasn’t led to any unifying conclusions about the etiology of the disease.”

    However, understanding MS as metabolic rather than an autoimmune begins to bring the disease and its causes into focus.

    THE LIPID HYPOTHESIS
    Corthals believes that the primary cause of MS can be traced to transcription factors in cell nuclei that control the uptake, breakdown, and release of lipids (fats and similar compounds) throughout the body. Disruption of these proteins, known as peroxisome proliferator-activated receptors (PPARs), causes a toxic byproduct of “bad” cholesterol called oxidized LDL to form plaques on the affected tissue. The accumulation of plaque in turn triggers an immune response, which ultimately leads to scarring. This is essentially the same mechanism involved in atherosclerosis, in which PPAR failure causes plaque accumulation, immune response, and scarring in coronary arteries.

    “When lipid metabolism fails in the arteries, you get atherosclerosis,” Corthals explains. “When it happens in the central nervous system, you get MS. But the underlying etiology is the same.”

    A major risk factor for disruption of lipid homeostasis is having high LDL cholesterol. So if PPARs are at the root of MS, it would explain why cases of the disease have been on the rise in recent decades. “In general people around the world are increasing their intake of sugars and animal fats, which often leads to high LDL cholesterol,” Corthals said. “So we would expect to see higher rates of disease related to lipid metabolism—like heart disease and, in this case, MS.” This also explains why statin drugs, which are used to treat high cholesterol, have shown some promise as an MS treatment.

    The lipid hypothesis also sheds light on the link between MS and vitamin D deficiency. Vitamin D helps to lower LDL cholesterol, so it makes sense that a lack of vitamin D increases the likelihood of the disease—especially in the context of a diet high in fats and carbohydrates.

    Corthals’s framework also explains why MS is more prevalent in women.

    “Men and women metabolize fats differently,” Corthals said. “In men, PPAR problems are more likely to occur in vascular tissue, which is why atherosclerosis is more prevalent in men. But women metabolize fat differently in relation to their reproductive role. Disruption of lipid metabolism in women is more likely to affect the production of myelin and the central nervous system. In this way, MS is to women what atherosclerosis is to men, while excluding neither sex from developing the other disease.”

    In addition to high cholesterol, there are several other risk factors for reduced PPAR function, including pathogens like Epstein-Barr virus, trauma that requires massive cell repair, and certain genetic profiles. In many cases, Corthals says, having just one of these risk factors isn’t enough to trigger a collapse of lipid metabolism. But more than one risk factor could cause problems. For example, a genetically weakened PPAR system on its own might not cause disease, but combining that with a pathogen or with a poor diet can cause disease. This helps to explain why different MS triggers seem to be important for some people and populations but not others.

    “In the context of autoimmunity, the various risk factors for MS are frustratingly incoherent,” Corthals said. “But in the context of lipid metabolism, they make perfect sense.”

    Much more research is necessary to fully understand the role of PPARs in MS, but Corthals hopes that this new understanding of the disease could eventually lead to new treatments and prevention measures.

    “This new framework makes a cure for MS closer than ever,” Corthals said.

    Source: Eurasia Review Copyright © 2011 Eurasia Review (23/12/11)

    © Multiple Sclerosis Resource Centre

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