Q. Why don’t we just get rid of the T-cells that damage the myelin sheets?
A. At first, we considered attacking T-cells to reduce possible autoimmune attacks on myelin sheaths. We rejected this idea because nonspecific targeting of T-cells could result in the extinction of crucial immune response pathways. After all, deactivating the T-cells would cause unwanted infections to spread even more rapidly. Meanwhile, the presence of cytokines would dilate the BBB and provide an environment for demyelination. This angle directed our project towards irreversibly binding and inhibiting cytokines. Because of their constant production and signaling in T cell attacks, their deactivation would pose far less immune disability.
Q. Why not use infrared signaling to control the release of remyelination drugs?
A. The use of infrared signaling to control the release of remyelination drugs was another idea we considered. In addition to cytokine binding receptors, newly researched remyelination stimulating medications would be contained inside small lipophilic nanoparticles capable of migrating through the BBB. Nanoparticles would be arranged in pairs: a nanosphere containing our desired drug, and a nanorod capable of being heated by near-infrared light. After injection of the module into the bloodstream, those that migrate towards the brain would be activated by light shining onto the targeted site of demyelination. Here, the heated nanorod would induce its partner nanoparticle to release both antibodies for cytokines and drugs that act on oligodendrocytes to promote remyelination. This idea was discarded for concerns over the safety of high-temperature reactions in patients’ brains and CNS. It also presented the further difficulty of moving nanoparticles of increasing size (such as with connected parts working in tandem) across the BBB. Although rejected, this idea directed our research attention towards using carrier-mediated transport to increase the accuracy of moving nanoparticles across the BBB.
Q. Why do we not use microvesicles? Why specifically nanotechnology?
A. We did consider injecting microvesicles that express antibodies for cytokines into an individual’s circulation. Some of these lipophilic microvesicles would diffuse across the BBB. Their antibody receptors would then bind and permanently disable cytokines. We rejected this design because the use of microvesicles would result in a number of uncontrollable variables. These include the inability to both efficiently dispose of unwanted microvesicles and monitor the rate at which they successfully cross the BBB. Microvesicle concentrations in the brain and CNS would rarely be coordinated with the need to slow down the immune response. These obstacles would likely render insignificant the inhibitory effects of cytokine-binding antibodies.
Q. Is there a potential consequence for using nanotechnology?
A. Like any other treatments, our medicine does have consequences. One point to keep in mind is the toxicity of nanotechnology if the medication is not conducted with proper care. In high concentrations, these nanotechnologies may end up causing unwanted chemical reactions creating biochemical damages within the human. Hence, guidelines and protocol will be placed to prevent such injuries.