Maybe if I'd added 'Rituximab' to the title of this thread it might gain more attention. Interesting article all the same. And of interest in our world I would think.
Seems that the strategy of blocking NMDA receptors (in order to reduce excitotoxicity) that many seem to advocate might not always be a good idea. I certainly get extremely brain-fogged from NMDA antagonists. Stimulating the NMDA might actually be a more viable option in these cases.
Interesting article, thanks Firestormm.
There seem to be a number of parallels with ME/CFS. (e.g. Rituximab, Herpes virus, and auto-immunity.)
Not that I read the Daily Wail you understand, Bob Charles flagged it on MEA Facebook earlier. Makes one think and I do like articles like that. It's all biology at the end of the day - however it's categorised.
She probably has an amalgam filling
It does depend on which antibodies you have :
Anti-NMDA receptor encephalitis and late onset autism are recently recognised and related autoimmune disorders involving antibodies to NMDA(glutamatergic) receptors with prodromal symptoms reminiscent of a viral infection and that result in a wide range of movement and neuropsychiatric symptoms and neuroinflammation. (Dalmau et al, 2011).
Autoimmune encephalitis (where symptoms include psychiatric features, confusion, memory loss and seizures followed by a movement disorder, loss of consciousness and autonomic fluctuations) and related disorders have also been associated with anti GABA-B receptor antibodies and/or glutamic acid decarboxylase (GAD – the enzyme responsible for converting glutamic acid to GABA) antibodies (Boronat et al, 2011). One recent hypothesis (Fitzgerald, Carter, 2011) proposes decreased GAD expression or activity as playing a key role in fibromyalgia.
Rituximab has also been used to treat anti-NMDA receptor encephalitis (Ikeguchi et al, 2012) supporting a close link between autoimmunity, glutamate/GABA and encephalitis.