A recent report in Science Traslational Medicine (1) has deserved a lot of attention by mainstream media. Headlines referred to it as the confirmation that narcolepsy is an autoimmune disease. Narcolepsy is an interesting disease both clinically (sleep attacks, cataplexy, sleep paralysis, visual hallucinations during early sleep and awakening…) and pathophysiologically. Current knowledge points at a selective death or damage in the neurons of the anterior part of the hypothalamus responsible of orexin production. Orexin (or hypocretin) is a secreted proteic neurotransmitter that regulates awakeness and apettite and whose levels in CSF are significantly lower in patients with narcolepsy than in controls. As usual, the exact cause of narcolepsy is unknown, although recent studies suggest that an autoimmune response, probably triggered by an environmental factor (let’s say, a virus), is the key process in its development (2).The paper by De la Herrán-Arita and colleagues reports an interesting, well-performed study that, contrary to what mainstream media say, does not demonstrate that narcolepsy is an autoimmune disease. But we’ll come to that later. The autoimmune hypothesis of narcolepsy is not new at all. Among the genes that have been associated to narcolepsy, most play important roles in the immune system (3). The strongest association was found with the HLA-DQB1*0602 allele, which more than 95% of the narcolepsy patients carry. But other genes, related to the immune system have also been implicated (4). However, as in any other complex disease, genes don’t explain everything. What the HLA system does is to present antigens (the targets of an immune response, regardless of it is against a pathogen or an autoimmune one) to T cells (lymphocytes) and T cells are the ones enabled to kill a cell carrying that antigen or to call other cells so they are the ones killing the antigenic cell. One
… require extraordinary evidence. That is the heading of a “Message from the Editor” in Annals of Neurology published online in April 2011. It comments on a paper demonstrating the absence of retroviral particles in CSF of patients with chronic fatigue syndrome while criticizes the role of publishers (and researchers) paying (too much) attention to breakthrough discoveries while they don’t care much about those same discoveries when they fail to be replicated. It also points out the role of mainstream media and the internet in amplifying these “extraordinary claims” and highlight the need of humble statements and careful replication before attracting mainstream media focus on those claims. They, as we did, compare the case with that of the CCSVI (the other way, though) and remember us the necessary slowness of science: ” […] as journal editors we have a responsibility to do everything possible to insure that data appearing in our pages will stand the test of time.” The only thing i don’t like in that necessary message is that it will remain within the limits of Annals of Neurology readers. That is the battle clinicians and researchers need to win. The one outside the official means. If we fail to convey this message out of our limits we will lose the battle against bad, harmful, attractive science. So the scientific community has to grow public but grow around our own environments, both our clinics and, more importantly, our communities.
AAN evidence based reviews don’t add anything new to what we probably know (or should know) or suspect about a treatment or intervention, but it’s always useful to have all data summarized to avoid the whole process of revision by oneself. In the last issue of Neurology journal we’ll find an evidence-based review about the use of plasmapheresis in neurological disorders. Not any surprise in GBS and CIDP being the diseases with a better level of evidence in plasmapheresis efficacy. Not anything to question, but just highlight a (small) paradox… One of the main mechanisms of action of plasmapheresis is pathogenic antibody removal, then, how can a well known antibody mediated disease like myasthenia have less evidence than those diseases in which cellular immunity is considered more important, such as MS or CIDP?
Taking a look around the internet, trying to find a blog/podcast/newsfeed/whatever, to discuss, learn and update about neuroimmunology i found almost nothing and decided to create this blog with that purpose. There may not be many neuroimmunologists out there but i think it’ll be enough if a few gather round this blog and comment what will come in the science and clinical practice of our field. So, anybody interested is welcome to provide information or even write posts, and every one out there is invited to join the discussion (if any).