Thursday, September 17, 2015
After a gap of almost 2 years, we are resurrecting this blog. A new and enthusiastic (not that last year's class weren't enthusastic, since some of them are continuing from last year) class of over 20 students has begun this academic year with the module on 'Molecular and Regenerative Medicine'. After prompting the class to come up with a topical news story that relates to the Mol and Regen Med module, Paul O'Shea suggested fampridine, since it was recently approved as a HSE-supported drug for the treatment of MS. In the US, fampridine is known as Dalfampridine (see paper by Alessandra Lugaressi, Pharmacology and clinical efficacy of dalfampridine for treating multiple sclerosis, Expert Opin. Drug Metab. Toxicol. (2015) 11(2):295-306), from which the Box 1 below is taken. Fampridine is administered orally twice a day, at a dose between 10 and 30 mg. Some side-effects have been noted, but these were not considered serious enough to disallow its use. The basis for its relevance relates to consequences of the stripping of myelin from CNS nerves during MS. During demyelination, potassium channels along the internode become exposed, allowing ions to leak out of the axon. This can interfere with normal nerve impulse conduction that occurs via sodium channels clustered at nodes of Ranvier. Fampridine can inhibit the slowly-inactivating potassium channels and does so by binding the cytoplasmic portion of the channel. Inhibition of potassium channel signaling increases the duration of the action potential, increasing transmitter release. Fampridine is hypothesised to have additional effects on non-neuronal cells, via potassium channels expressed on them. These cells include glia as well as immune cells Guidance on the use of fampridine have been provided by MS Ireland and this information can be found at the following here.