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    You are here : Home » MS Research News » Brain Inflammation

    Brain Inflammation

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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.

    Possible multiple sclerosis progression breakthrough announced

    Brain InflammationUniversity of Adelaide scientists have revealed breakthrough research that has the potential to help prevent the progression of multiple sclerosis.

    The researchers successfully halted the autoimmune disease in mice.

    They hold great hope the same results can be reproduced among humans. MS Research Australia research development manager Dr Lisa Melton said the study results were "extremely exciting".

    MS is a progressive disease where the body attacks its own central nervous system, causing nerve inflammation and scarring. It results in the impairment of motor, sensory and cognitive function.

    Dr Melton said it provided fresh hope for the 23,000 MS sufferers in Australia.

    "It won't be a cure but it's another avenue by which we can reduce the inflammation which damages the brain and spinal cord," she said.

    "If this approach works in humans, it would stop the inflammation," she said.

    "But it won't undo any damage to the nerves which has already occurred."

    In animal trials, Dr Iain Comerford and colleagues at the university successfully prevented the progression of MS by inhibiting the molecule, known as PI3Kgamma, which activates the cells that cause the immune system to attack itself and cause the nerve damage.

    The same molecule has been successful in other autoimmune disorder trials.

    Human trials were underway in other labs around the world, but any drug would be at least five years away, Dr Comerford said.

    "In the animal model, it was preventive and also we could reverse the disease, but it remains to be seen whether that also happens in human beings," he said.

    He said the damage in MS patients was caused by white blood cells moving into and attacking the central nervous system.

    "We've inhibited an enzyme, PI3Kgamma, which is involved in the activation and migration of white blood cells," Dr Comerford said.

    "The white blood cells have to move from the blood into the nervous system to do damage in MS.

    "By doing that, we reduce the activation of the white blood cells and reduce the migration of the cells into the central nervous system."

    Dr Comerford and his team found that when PI3Kgamma was present, severe damage to myelin, which insulates the nerves, was evident, resulting in inflammation in the spinal cord and myelin loss.

    The patient's immune system would still function and provide immune responses which protect against infection.

    He said that none of the existing drugs for MS patients was completely effective.

    Dr Comerford's research, which was published in the journal PLOS One, was completed under a three-year fellowship from MS Research Australia.

    Dr Melton said the research delivered a more targeted approach, than existing drugs used to treat MS.

    "We've got drugs that do really well at reducing the relapses which occur in MS but nothing is perfect," she said. "They all have side-effects," she said.

    Source: Herald Sun © Herald & Weekly Times Pty Limited (03/10/12)

    Protein offers hope for MS and Alzheimer's disease

    Translocator ProteinA single protein implicated in inflammatory brain diseases, including multiple sclerosis and Alzheimer’s disease, could lead to novel treatments and better diagnoses.

    Scientists at the Australian Nuclear Science and Technology Organisation (ANSTO) are using a technique called neutron reflectometry to study the translocator protein, which is responsible for transporting molecules across mitochondrial membranes.

    The translocator protein is found in cells throughout mammal tissue and is believed to play a number of important roles, including in stress regulation. Its presence in the brain, however, is a sign of inflammation, which can be caused by injury or a number of diseases such as multiple sclerosis and Alzheimer’s disease.

    "Virtually not there in healthy brains"

    “[The translocator protein] is virtually not there in healthy brains, but then suddenly it appears when there’s brain inflammation, which implies it could be quite important,” explained Claire Hatty, a biophysicist who is involved with the ANSTO research for her PhD.

    A paper on the research – which is still in its preliminary stages – will be published in ANSTO Research Selections 2012, due for publication within the next month.

    Neutron reflectometry involves firing neutrons at an object, in this case a synthetic cell membrane embedded with the protein. The technique allows researchers to non-invasively penetrate the surface of the cell membrane and closely study its structure.

    “We’re using techniques that have traditionally been used in physics, so I find it interesting how we can apply them to biology,” added Hatty.

    As part of her PhD research, Hatty hopes to get a closer look at how the translocator protein interacts with drugs on the molecular scale.

    New drugs, better imaging for brain inflammation

    “Because this protein appears during the inflammatory process that contributes to diseases such as multiple sclerosis, if we can better understand what it is doing and how it’s contributing to that process, we might eventually be able to create drugs that can modulate the process and even reduce the inflammation,” she said. “It’s far-reaching, but it’s what we’re hoping for.”

    Other ANSTO researchers are also using the protein for its imaging potential, to scan for brain inflammation. This could be useful as a marker for diseases such as Alzheimer’s, and to scan inflammation caused by brain injuries.

    “Processes of neuro-degeneration, such as Alzheimer’s disease, are accompanied by inflammation, so the protein has been used to track brain inflammation before there’s any loss of neurons,” said Hatty.

    The result could be earlier diagnosis – and ideally treatment – of Alzheimer’s disease, before symptoms set in.

    “Almost all brain diseases have an inflammatory component and the translocator protein is thought to play an important role in this process,” commented Steve Meikle, a medical imaging physicist at the University of Sydney, who was not involved with the ANSTO research.

    “This research is providing new insights into the structure and function of this important protein, which will ultimately help the developers of new drugs in their quest to produce more effective treatments for brain diseases such as multiple sclerosis,” he said.

    “It will also help the development of new imaging tools that detect inflammation in the brain during the very early stages, when treatment can be most effective.”

    Source: Cosmos ©2006-12 Luna Media Pty Ltd (30/08/12)

    Inflammation in brain inhibited by new class of potential drugs

    MRIScientists at Emory University School of Medicine have identified a new group of compounds that may protect brain cells from inflammation linked to seizures and neurodegenerative diseases.

    The compounds block signals from EP2, one of the four receptors for prostaglandin E2, which is a hormone involved in processes such as fever, childbirth, digestion and blood pressure regulation. Chemicals that could selectively block EP2 were not previously available. In animals, the EP2 blockers could markedly reduce the injury to the brain induced after a prolonged seizure, the researchers showed.

    The results were published online this week in the Proceedings of the National Academy of Sciences Early Edition.

    "EP2 is involved in many disease processes where inflammation is showing up in the nervous system, such as epilepsy, stroke and neurodegenerative diseases," says senior author Ray Dingledine, PhD, chairman of Emory's Department of Pharmacology. "Anywhere that inflammation is playing a role via EP2, this class of compounds could be useful. Outside the brain, EP2 blockers could find uses in other diseases with a prominent inflammatory component such as cancer and inflammatory bowel disease."

    Prostaglandins are the targets for non-steroid anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen. NSAIDSs inhibit enzymes known as cyclooxygenases, the starting point for generating prostaglandins in the body. Previous research indicates that drugs that inhibit cyclooxygenases can have harmful side effects. For example, sustained use of aspirin can weaken the stomach lining, coming from prostaglandins' role in the stomach. Even drugs designed to inhibit only cyclooxygenases involved in pain and inflammation, such as Vioxx, have displayed cardiovascular side effects.

    Dingledine's team's strategy was to bypass cyclooxygenase enzymes and go downstream, focusing on one set of molecules that relay signals from prostaglandins. Working with Yuhong Du in the Emory Chemical Biology Discovery Center, postdoctoral fellows Jianxiong Jiang, Thota Ganesh and colleagues sorted through a library of 262,000 compounds to find those that could block signals from the EP2 prostaglandin receptor but not related receptors. One of the compounds could prevent damage to neurons in mice after "status epilepticus," a prolonged drug-induced seizure used to model the neurodegeneration linked to epilepsy. The team found that a family of related compounds had similar protective effects.

    Dingledine says that the compounds could become valuable tools for exploring new ways to treat neurological diseases. However, given the many physiological processes prostaglandins regulate, more tests are needed, he says. Prostaglandin E2 is itself a drug used to induce labor in pregnant women, and female mice engineered to lack the EP2 receptor are infertile, so the compounds would need to be tested for effects on reproductive organs, for example.

    Source: Medical News Today © MediLexicon International Ltd 2004-2012 (17/02/12)

    © Multiple Sclerosis Resource Centre (MSRC)

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