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New Potential Therapeutic Strategy to Halt Disease Progression in Multiple Sclerosis Developed

May 21, 2015

A new study recently published in the journal Annals of Neurology revealed a potential new therapeutic strategy to halt multiple sclerosis (MS) disease progression. The study is entitled “Melanoma cell adhesion molecule–positive CD8 T lymphocytes mediate central nervous system inflammation” and was led by researchers at the CanadianUniversité de Montreal, the Centre de Recherche du Centre Hospitalier de l’Université de Montréal (CRCHUM), and the Centre Hospitalier de l’Université de Montréal (CHUM)–Notre Dame Hospital.

MS is a progressive neurodegenerative autoimmune disorder that results from an attack on the central nervous system by the body’s own immune system, causing inflammation and damage to the myelin layer that covers and protects nerve fibers. Myelin loss leads to impairment in signal transmission along the nerve fibers, affecting motor function (like coordination, balance, speech and vision), causing irreversible neurological disability and paralysis. It is estimated that more than 2.3 million people in the world suffer from the disease. In Canada, nearly 75,000 people have MS, and in the US, it is estimated that up to 400,000 people have the disease.

The blood brain barrier protects the brain from external attacks, and it can prevent the entry of immune cells such as lymphocytes (a type of white blood cell) into the central nervous system. However, in MS patients, the blood brain barrier protection is often leaky, allowing the passage of two types of lymphocytes into the nervous system, CD4 and CD8. These lymphocytes destroy the myelin layer leading to a decrease in nerve impulse transmission.

The research team had previously discovered a cell adhesion molecule known as MCAM (melanoma cell adhesion molecule) that was found to play a key role in the deregulation of the immune system seen in MS patients. Now, using human samples and mice models, researchers discovered that the blockade of MCAM expression in lymphocytes could lead to a delay in disease onset and significantly slow disease progression.

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