Abstract: Computational Model of NF-κB

Multiple Sclerosis (MS) is an autoimmune neurodegenerative disease that cannot be cured. MS causes the body’s own immune system to attack the axons of neurons, disrupting communication between the brain and the body. The result is symptoms in patients like demyelination, loss of muscle coordination, and vision loss. NF-κB (Nuclear factor kappa B) is a transcriptional factor widely known as the centerpiece of transcriptional regulation for inflammatory and autoimmune pathways. The cyclical nature of NF-κB and its pivotal role in the disease makes it a prime candidate to study using a computational approach. Using kinetics data and molecular biology studies, an accurate model of the exact role that NF-κB plays in the disease can be created. This model is malleable not only to mitigating disease factors, but also to a wide variety of treatments that can alter the general state of the disease. The goal of the project is to produce a finished model of the large network of related proteins and cells and to program the kinetics in MATLAB to study the potential of targeting the NF-κB pathway for treatment.

A Computational Model including Role of NF-κB in Multiple Sclerosis

Multiple Sclerosis (MS) is an autoimmune, neurodegenerative disease that cannot be cured. The disease causes the body’s own immune system to attack the axons of neurons, disrupting communication between the brain and the body. Those afflicted with Multiple Sclerosis slowly lose the ability to send signals down their axons. Consequently, they are no longer able to function or use those parts of their nervous system, and in many cases become immobile. The mechanism for axonal degradation is not properly understood, but a variety of pathways and factors have been discussed as contributing towards the degradation. NF-κB is a well-known transcription factor that can be cited as the “master switch” for immune response, and can be known to alter the behavior in immune cells’ response to injury and function. In the context of MS, NF-κB controls the macrophage phenotype that is expressed.

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