It can cause blackouts, memory loss, and hallucinations. It’s typically diagnosed in people in their 20s and considered more common among women than men. It’s not schizophrenia, but it can be misdiagnosed as such. This week At the Lab, CSHL Professor Hiro Furukawa returns to speak about anti-NMDAR encephalitis, an autoimmune disease discovered less than 20 years ago.
Read the related story: Putting out a brain on fire
Transcript
Nick Wurm: You’re now At the Lab with Cold Spring Harbor Laboratory. My name is Nick Wurm, and this week At the Lab, “Dancing with fire.”
NW: Right now, nerve cells inside your brain are firing off signals called electrical impulses. These signals play a role in virtually everything you do, including listening to podcasts. For electrical impulses to travel between nerve cells, they need to pass through protein molecules called brain receptors.
NW: CSHL Professor Hiro Furukawa has dedicated his career to studying an important class of brain receptors known as NMDARs. If you caught Furukawa on our podcast last season, you might remember how he described NMDARs’ movement.
Hiro Furukawa: We’re basically just figuring out how the NMDA receptor dances around to open and close the ion channel. They literally dance around.
NW: Furukawa has been studying NMDAR dysfunction in the context of Alzheimer’s and other neurodegenerative diseases. Recently, however, he became aware of an autoimmune disorder called anti-NMDAR encephalitis. Furukawa breaks it down like this.
HF: What these autoimmune antibodies do is bind to these critical NMDA receptors and inhibit them so the neurons can no longer generate the electrical patterns that we need for normal activities. The consequence is what we call encephalitis. That’s brain inflammation.
NW: Anti-NMDAR encephalitis was first discovered in 2007. In one popular case, a patient said it felt like her brain was on fire.
HF: That’s one symptom. But along with that, it causes schizophrenia-like symptoms including memory loss.
NW: In fact, before receiving her diagnosis, the patient thought she was suffering from bipolar disorder. Furukawa thinks hers might not be the only such case.
HF: Could, for example, some schizophrenic patients have this disease? Could it be caused by antibodies? There are so many possibilities like that. So, we need to have a way to isolate those antibodies and diagnose them—assessing the binding patterns at the molecular level. This is the first time anybody’s demonstrating a workflow for this.
NW: Furukawa’s lab successfully isolated patient antibodies in three cases of anti-NMDAR encephalitis. They saw different binding patterns in each patient. There were also variations in symptoms among the three patients. If scientists can connect these differences, clinicians may one day be able to offer more personalized diagnoses and therapies. But there’s more.
NW: Right now, more than 3 billion people around the world are living with neurological conditions. Many do not respond to treatment. For some, this research could finally explain why.
NW: Thanks again for joining us At the Lab. If you like what you heard, remember to hit subscribe and visit CSHL.edu for more fascinating science stories like this one. For Cold Spring Harbor Laboratory, I’m Nick Wurm, and I’ll see you next time At the Lab.