Pipeline & Disease Focus

Multiple Sclerosis

Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the CNS that usually begins in young adulthood. It is characterized by lesions within the CNS and demyelination is a key feature of these lesions. There is also evidence of axonal transection or axonal degeneration. Genetic and environmental factors confer susceptibility to MS, as shown by epidemiological studies. These factors include gender, race, exposure to infections (particularly during childhood and adolescence), and geographical variables such as latitude and sun exposure. The clinical symptoms vary depending on the parts of the CNS affected – they include focal neurological deficits such as motor weakness or paralysis, sensory loss, loss or blurring of vision and cognitive deficits.

The etiology of MS remains unknown; however, data from MS lesions, genetic susceptibility, the use of immunotherapies and extensive studies on animal models of MS suggest that it is an immune-mediated disease. Autoreactive T cells are thought to initiate an autoimmune response directed against components of CNS myelin. There is also thought to be a role for antibody-mediated responses to myelin antigens in disease pathogenesis. Although primary demyelination is considered a key feature of MS, extensive axonal pathology is also present. Postmortem analysis of brains of MS patients demonstrated axonal transection in both active and chronic lesions, the frequency of which was related to the degree of inflammation . Furthermore, loss of parental cell bodies in the cortex has also been observed. Experimental autoimmune encephalomyelitis (EAE), an animal model of MS induced by immunization with myelin components in adjuvant substances, shows comparable neuronal pathology, which renders this model suitable for both neuro- and immunopathological studies of autoimmune inflammatory demyelination.

TThere has been several approaches to treating MS. However, none so far has been able to treat the disease. We believe Bioniz technology would be able to intervene with the action of multiple cytokines that affect T-cell- as well as NK-mediated autoimmunity and hence prevent the disease progression.

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