Researchers Identify Molecular Key for Delaying Progression of Multiple Sclerosis


Researchers from University of the Basque Country improve the symptoms in the chronic phase of multiple sclerosis in lab experiments.

Multiple Sclerosis is an autoimmune disease that attacks and destroys a structure known as the “myelin sheath,” whose integrity is indispensable for the brain and spinal cord to function properly. Current therapies that aid in treatment of multiple sclerosis are based on modulating the activity of the immune system or preventing its cells from accessing the central nervous system and damaging it. However, these therapies are effective in the early phases and do not prove beneficial as the disease progresses and leads to functional deterioration. The microglial cells in the brain, which primarily cause chronic inflammation that is responsible for the neurological deterioration during the progressive phase of the disease. These microglial cells are the brain’s sentries that respond when faced with any damage or infection in it. This principally beneficial mechanism turns harmful when it is prolonged over time. It eventually leads to chronic inflammation, which aggravates the disease and encourages its progression.

The researchers identified a receptor known as P2X4 present in the microglial cells. It is responsible for increasing anti-inflammatory potential of the microglial cells in order to reduce the damage in multiple sclerosis. Furthermore, it was observed that it encourages the body’s own repair responses. Animal models of the disease were used for the experimental development to discover that the drugs that activate P2X4 to improve the symptoms during the chronic phase of the disease. Dr. María Domercq of the Department of Neurosciences, stated that the finding are expected to open a new channel of pharmacological development for the treatment of Multiple Sclerosis. The research published in the journal EMBO Molecular Medicine on July 04, 2018, was coordinated by the Basque Autonomous Community.


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