(Mémoire de) maîtrise (master)
Detecting IL-26 in multiple sclerosis patients by ELISA
DU PASQUIER R.
Université de Lausanne, Faculté de biologie et médecine
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Multiple sclerosis (MS) is an auto‐inflammatory disease of the central nervous system (CNS) that eventually leads to neuro‐degeneration. MS affects over one million people worldwide, twice as many women as men, and is the first cause of neurologic disability in young adults(1). For the patient, the diagnosis of MS means a sentence to hardship, a storm of uncertain hopes and incomprehensible certainty about future loss of function. MS is a progressive disease that can take various clinical courses. In most cases, there is a progression towards accumulation of neurological dysfunction with relapses and remissions (RR‐MS). During relapses, symptoms commonly include a loss of sensation, coordination or vision. In the beginning of the disease, there is usually restitution ad integrum of neurological functions, but over time, neurological impediments persist even during the remission phases. Thus, the functional losses accumulate as the disease progresses to a second phase (Secondary Progressive [SP‐MS]). In ten percent of cases, the disease is progressive from the beginning, without remissions (Primary Progressive MS [PP‐MS])(2). In about a quarter of patients, the progression will never lead to major disability, while in some patients the course of the disease quickly evolves towards major functional loss(3), thereby making it a highly unpredictable and heterogeneous disease. The precise cause(s) of MS is/are undetermined, which explains why no curative treatment has so far been developed. There is therefore a huge interest in understanding the immunopathogenesis of MS, as so much is still to be learnt about this autoinflammatory and degenerative disorder of the CNS.
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