Epub: Cambron M et al..Fluoxetine in Progressive Multiple Sclerosis (FLUOX-PMS): study protocol for a randomized controlled trial. Trials. 2014; 15:37.
BACKGROUND: Fluoxetine might theoretically reduce axonal degeneration in MS because it stimulates energy metabolism through enhancing glycogenolysis*, stimulates the production of brain-derived neurotrophic factor**, and dilates cerebral arterioles. The current document presents the protocol of a clinical trial to test the hypothesis that fluoxetine slows down the progressive phase of MS.
brain-derived neurotrophic factor (BDNF) = is a growth factor. BDNF acts on certain neurons of the central and peripheral nervous system helping to support the survival of existing neurons, and encourage the growth and differentiation of new neurons and synapses. Synapses are the connections between neurones; they convert an electrical into a chemical signal.
METHODS: The FLUOX-PMS trial is a multi-center, randomized, controlled and double-blind clinical study. A total of 120 patients with the diagnosis of either secondary or primary progressive MS will be treated either by fluoxetine (40 mg daily) or placebo for a total period of 108 weeks.
DISCUSSION: The FLUOX-PMS trial will gives us information as to whether fluoxetine has neuroprotective effects in patients with progressive MS.Trial Registration: Eudra-CT: 2011-003775-11.
A new way for Neuros to get publications is to tell us what they are going to do, when you are only interested to know what was done and found. The difference between the two is a number of years Maybe scientists should start a journal and call it “Experiment”. However they may get scooped. Someone else may do it quicker.
Anyway, as you say not enough is being done about progressive MS, I thought I would post about this.
Fluoxetine is frequently used to treat major depression and is an SSRI selective serotonin re-uptake inhibitor also known as Prozac this follows on from earlier studies in less than 50 MSers where it was suggested that “at least 200 patients would have been needed to detect a 50% treatment effect so is this study adequately powered. It is suggested that fluoxetine stimulates astrocytic glycogenolysis, which serves as an energy source for axons, may be good thing to do, let’s hope so.